MIDTERM 2 (L09-L17) Flashcards

1
Q

What is sensation?

A

It refers to how cells of the nervous system detect stimuli in the environment (such as light, sound, heat, etc.), and how they transduce these signals into a change in membrane potential and neurotransmitter release

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2
Q

What is perception?

A

It refers to the conscious experience and interpretation of sensory information

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3
Q

what are sensory neurons?

A

also known as Sensory Receptors

they are specialized neurons that detect a specific category of physical events

they express receptor proteins that are sensitive to a specific feature of the external environment, such as
- the presence of specific molecules (via chemical interactions)
- smell, taste, nausea, pain
- physical pressure
- touch, stretch, vibration, acceleration, gravity, balance, hearing, thirst, pain
- temperature
- heat, cold, pain
- pH (acidity, basicity)
- sour taste, suffocation, pain
- electromagnetic radiation (light)
- vision

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4
Q

what are some other senses that non-human animals have?

A

examples:
- the ability to detect electrical and magnetic fields, humidity, and water pressure

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5
Q

what is sensory transduction?

A

process by which sensory stimuli are transduced (converted) into receptor potentials

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6
Q

What is a receptor potential?

A

Graded change in the membrane potential of a sensory neuron caused by sensory stimuli

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7
Q

What is a sensory neuron?

A

Specialized neuron that detects a particular category of physical events (sensory stimuli)
- e.g., photoreceptor (cells) transduce light into receptor potentials

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8
Q

what don’t all sensory neurons have?

A

not all sensory neurons have axons or action potentials, but they all release neurotransmitter

the sensory neurons that do not have action potentials releases neurotransmitter in a graded fashion, dependent on their membrane potential

The more depolarized they are, the more neurostransmitter they release

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9
Q

What are opsins?

A

Receptor proteins that are sensitive to light

the opsins in our eyes gain their sensitivity to light by binding a molecule of retinal

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10
Q

What are the four different types of opsin proteins we use to detect light?

A

rhodopsin
red cone opsins
green cone opsins
blue cone opsins

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11
Q

What are the four different photoreceptor cells in our eye?

A

Each photoreceptor cell in our eye contains only one kind of opsin protein, so we have four different types of photoreceptor cells:
- rod cells express rhodopsin protein
- red cone cells express the red cone opsin
- green cone cells express the green cone opsin
- blue cone cells express the blue cone opsin

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12
Q

what is a photoreceptor cell?

A

the sensory neuron responsible for vision
- they transduce the electromagnetic energy of visible light into receptor potentials

the human retina contains 4 types of photoreceptor cells; each expresses a different type of opsin protein

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13
Q

What is retinal?

A

small molecule (synthesized from vitamin A) that attaches to the opsin proteins in our eye

the retinal molecule is what actually absorbs the electromagnetic energy of visible light in our eyes

The wavelength of light it can detect depends on the opsin protein it is attached to

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14
Q

What type of receptors are the opsins in our photoreceptor cells? (ionotropic or metabotropic)

A

inhibitory metabotropic receptors

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15
Q

What does visible light refer to?

A

It refers to electromagnetic energy that has a wavelength between 380 and 760 nm

we detect this light using four kinds of photoreceptor cells (1 rod cell and 3 cone cells)

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16
Q

What is trichromatic coding?

A

The three cone opsins are sensitive to different wavelengths of light:
- blue cone opsins are most sensitive to short wavelengths
- green cone opsins are most sensitive to medium wavelengths
- red cone opsins are most sensitive to long wavelengths

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17
Q

What is color perception a function of?

A

Colour perception is a function of the relative rates of activity in the three types of cone cells (i.e., colours are discriminated by the ratio of activity across the three types of cones)

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18
Q

What does the amount that any cone will be activated depend on?

A

The amount that any one cone will be activated depends both on the wavelength of the light and the amount of it (its intensity)

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19
Q

If shown three colours separately (blue, green, and red) at the same intensity, what colour do people often say is the brightest?

A

green, because green cone opsins are the most sensitive to light

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20
Q

Why is paint different than light?

A

Paint doesn’t create light; its absorbs some and reflects some

When it comes to painting, yellow, magenta, and cyan are the three primary colours because each of these dyes only absorb (subtracts) one colour from white light

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21
Q

What happens when you mix chemicals that absorb all wavelengths of visible light?

A

you end up with a black piece of paper

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22
Q

What are the three dimensions of our perception of light?

A

brightness - intensity (luminance, amount)

saturation - purity (in terms of composite wavelengths)

hue - dominant wavelength (colour)

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23
Q

What happens when brightness is 0%?

A

Your image will be black

hue and saturation have no impact if there is no brightness

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24
Q

What happens when saturation is 0%?

A

You are in the middle of the colour cone where there is no colour (equal contribution from all wavelengths) which means you have a black and white image

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25
what is protanopia?
absence of the red cone opsin (1% of males) visual acuity is normal because red cone cells get filled with green cone opsin people with this inherited condition have trouble distinguishing colours in the green-yellow-red section of the spectrum simple mutations in the red cone opsin (1% of males) produce less pronounced deficits in colour vision mutation in the red cone opsin hinder colour vision if they make the red cone opsin act more like the green cone opsin (in terms of what light it can detect)
26
What is tritanopia?
absence of the blue cone opsin (1% of the population) blue cone cells do not compensate for this in any way, but the blue cone opsin is not that sensitive to light anyway, so visual acuity is not noticeably affected
26
What is deuteranopia?
absence of the green cone opsin (1% of males) visual acuity is normal because green cones get filled with red cone opsin - people with this inherited condition have trouble distinguishing colours in the green-yellow-red section of the spectrum simple mutation of the green cone opsin (6% of males) produce less pronounced deficits in colour vision
27
What is true colour blindness called?
achromatopsia it is typically caused by mutations in the g protein signalling cascade that is similar in all cone cells
28
Why do cone cells encode colour vision?
cone cells are not particularly sensitive to light, but because there are three different kinds of them, each sensitive to different wavelengths, they encode colour vision
29
What is the cornea?
the outer, front layer of the eye it focuses incoming light a fixed amount
30
What is the iris?
it's a ring of muscle the contraction and relaxation of this muscle determines the size of the pupil, which determines how much light enters the eye
31
What is the conjuctiva?
it is a mucous membrane that lines the eyelid
32
what is the sclera?
it is opaque and does not permit entry of light the white part of the eyeball
33
What is the lens of the eye?
the lens consists of several transparent layers the shape of the lens can change to allow the eye to focus, a process known as accomodation
34
What is the retina?
the interior lining (furthest back part) of the eye is the retina the retina contains photoreceptor cells in humans, photoreceptor cells are classified as rod or cone cells
35
what is the vitreous humour?
light passes through the lens and crosses the vitreous humour, a clear, gelatinous fluid
36
What is the fovea?
the central region of the retina is the fovea there is very little compression of visual information in the fovea, so this is where we have the highest visual acuity primarily contains cone cells, each of which connects to a single bipolar cell, which in turn connect to a single ganglion cell - thus, photoreceptors in the fovea can register the exact location of the light, enabling high resolution, colour vision
37
What is the optic disk?
it is where the optic nerve exits through the back of the eye there are no photoreceptors here, so it is a blind spot in our eye
38
What are the three different neurons in the retina?
photoreceptors bipolar cells ganglion cells
39
What kind of cells are found in the periphery of the retina?
In the periphery, many rod cells (containing rhodopsin) converge onto fewer and fewer downstream collections of neurons (bipolar and ganglion cells) With this compression of information, there is little information about the exact location and shape of the light in peripheral vision, but we can easily detect dim light, moving lights, and general shapes
40
What is fovea vision sensitive to?
detail and colour (high resolution colour vision)
41
What is peripheral vision sensitive to?
dim light (low resolution grayscale vision)
42
What do images deficient in high frequency information look like?
unfocused, but we can still make out the form
43
How is the high visual acuity needed for reading made possible?
The high visual acuity needed for reading is only possible in the fovea, which is primarily where the cone cells are located
44
What muscles move the eye around and hold it in place in the orbit?
Six extraocular muscles are attached to the sclera: the tough, outer white of the eye
45
What are the two different types of movement of the eye?
saccadic movements - rapid, jerky shifts in your gace from one point to another - our eyes scan a scene by making saccadic movements pursuit movements allows us to maintain an image of a moving object
46
what are bipolar cells?
neurons that relay information from photoreceptor cells to ganglion cells
47
what are ganglion cells
the only neurons in the retina that send axons out of the eye they receive information from bipolar cells and project to the rest of the brain; their axons give rise to the optic nerve, which leaves the retina through the optic disk (i.e., the blind spot of the retina)
48
What are horizontal cells?
neurons that interconnect and regulate the excitability of adjacent photoreceptor and bipolar cells they adjust the sensitivity of these neurons to light in general
49
what are amacrine cells?
neurons that interconnect and regulat the excitability of adjacent bipolar and ganglion cells there are many different types of amacrine cells, and each have different functions
50
in addition to the regular leak potassium ion channels that all neurons have, what do photoreceptor cells express?
they express "leaky" sodium ion channles which are open in the dark (when the cells are at rest)
51
What happens in the dark to photoreceptor cells?
in the dark, sodium continually enters through these ion channels, which depolarizes the photoreceptor cell membrane to -40 mV at this depolarized membrane potential, photoreceptor cells continuously release glutamate
52
What happens when the retinal portion the retinal-opsin complex absorbs light?
it causes a conformational change (change in shape) in the opsin receptor protein this launches a g-protein signalling cascade that closes the open sodium ion channels the closing of these channels hyperpolarizes the membrane to -70 mV, at which point the photoreceptor cell largely stops releasing glutamate so, photoreceptor cells are more depolarized and release more glutamate in the dark than in the light
53
What are the two main kinds of bipolar cells?
OFF bipolar cell - express ionotropic glutamate receptors, so they are depolarized by glutamate - because photoreceptor cells release glutamate in the dark, OFF bipolar cells are more active (more depolarized) in the dark than in the light ON bipolar cells - only have inhibitory metabotropic glutamate receptors, so they are uncommonly inhibited by glutamate - thus, ON bipolar cells are more active (more depolarized) in the light vs. the dark
54
What type of neurons are ganglion cells in the retina?
retinal ganglion cells (RGCs) are typical neurons they have action potentials and are generally excited by glutamate
55
What are receptive fields?
the receptive field of a neuron involved in visual processing is defined as the area of visual space where the presence of light influences the firing rate of that neuron (i.e., the part of space in which light must fall to get a response from the neuron)
56
How do you identify the receptive field of a particular neuron?
you record from the neuron as the animal maintains focus on a central fixation point you then shine light in different areas of visual space (e.g., near or far from the fixation point in any direction, usually on a computer screen) and see where in visual space a change in light alters the spiking activity of the neuron
57
What is the first cell in the pathway of a receptive field?
when the correct wavelength of light is presented in a photoreceptor cell's receptive field, the photoreceptor cell hyperpolarizes and becomes less active (releases less glutamate)
58
What is the second cell in the pathway of a receptive field?
there are two main types of bipolar cells (ON & OFF) when light is presented in the receptive field of ON bipolar cells, they depolarize and release more glutamate when light is presented in the receptive field of OFF bipolar cells, they hyperpolarize and release less glutamate They respond differently to the changes in photoreceptor cell activity because they have different kinds of glutamate receptors - ON bipolar cells only have inhibitory glutamate receptors; OFF bipolar cells have excitatory glutamate receptors
59
What is the third cell in the pathway of a receptive field?
retinal ganglion cells generally integrate information from many ON and OFF bipolar cells their receptive fields often have a "center-surround" organization, and they are called ON or OFF cells, depending on whether they show increased or decreased spiking activity when light is presented in the center of their receptive field ON cells are excited by light in the center and are inhibited by light in the surorund OFF cells are excited by light in the surround and are inhibited by light in the center
60
Visual information is relayed from where to where?
visual information is relayed from retinal ganglion cells (RGCs) to the thalamus (the lateral geniculate nucleus) to area V1 in the ceberal cortex (primary visual cortex) the receptive fields of V1 neurons are the sum of many RGCs
61
What are are simple cells in the primary visual cortex?
Simple cells in primary visual cortex are sensitive to lines of light, and their receptive fields are typically organized in a center-surround fashion
62
What is the primary visual cortex?
Also known as area V1 or striate cortex neurons in V1 have larger receptive fields than the retinal ganglion cells - they are most activated when a line of light in a particular orientation is detected in the receptive field cells respond best when a line is in a particular position - a particular orientation some neurons respond best to vertical lines, some to horizontal lines, and some to lines oriented somewhere in between
63
What are neurons in the eye trying to identify?
every little spot in your visual field is rigorously analyzed is there light in that spot and is it oriented this way or that way? the neurons are trying to identify areas where there are sharp transitions between light and dark (or between two colours) the neurons are trying to identify borders, edges, corners Neurons downstream of V1 are going to put all this information together to identify objects and their relative position in space
64
what is considered the visual association cortex?
All of the occipital lobe surrounding primary visual cortex is considered visual association cortex visual association cortex extends into the parietal and temporal lobes, forming respectively the dorsal and ventral streams of visual information processing
65
What is the "where" visual stream of the brain?
The dorsal stream of visual information starts in primary visual cortex and ends in posterior parietal cortex it is involved in identifying spatial location it encodes where objects are, if they are moving, and how you should move to interact with them or avoid them
66
What is the "what" visual stream in the brain?
the ventral stream starts in primary visual cortex and ends in inferior temporal cortex it is involved in identifying form (shape) It encodes what the object is and its colour
67
what is monocular vision?
some V1 neurons respond to visual input from just one eye
68
What is binocular vision?
Most V1 neurons respond to visual input from both eyes
69
What is depth perception?
there are many monocular cues that can be used to estimate depth, such as relative size, amount of detail, relative movement as we move our eyes, etc. these are the cues we use to appreciate depth when looking at a 2-dimensional image (e.g., on a photograph or TV screen)
70
What is stereopsis?
The perception of depth that emerges from the fusion of two slightly different projections of an image on two retinas the difference between the images from the two eyes is called retinal disparity it results from the horizontal separation of the two eyes it improves the precision of depth perception, which is particularly helpful when trying to quickly plan movements to interact with objects moving in space
71
What is an agnosia?
An agnosia is a deficit (problem) in the ability to recognize or comprehend certain sensory information, like specific features of objects, people, sounds, shapes, or smells, although the specific sense is not defective nor is there any significant memory loss
72
What does agnosia relate to?
An agnosia relates to a problem in some sensory association cortex (typically in a single sensory modality) - not to problems that relate to the sensory neurons themselves or to the primary sensory areas example: visual agnosia relates to damage located downstream of primary visual cortex (in visual association cortex, or the dorsal visual stream in the parietal cortex, or the ventral visual stream in the temporal cortex)
73
What is akinetopsia?
a type of visual agnosia caused by damage in an area of the dorsal visual stream (in the parietal lobe of the cerebral cortex) it is a deficit in the ability to perceive movement
74
What is cerebral achromatopisa?
in contrast to regular achromatopsia, which is complete colour blindness due to defective cone opsin signalling, cerebral achromatopsia is a visual agnosia caused by damage to the ventral visual stream people with cerebral achromatopsia deny having any perception of colour they say everything looks dull or drab, and that it is all just "shades of grey" - people with regular achromatopsia don't say those things, because they have no conception of colour
75
What is prosopagnosia?
failure to recognize particular people by sight of their faces; caused by damage to the fusiform gyrus (fusiform face area)
76
What does descending neural activity from the top areas reflect?
to some extent, descending neural activity from the top areas reflect predictions about what the input is most likely be in the next moment (based on previous experience) this descending information cancels out the correctly predicted ascending information, so the only information that actually ascends are errors in visual predictions
77
how do feedback connections function in the visual cortex wiring diagram?
each level of the network (except the lowest level, which represents the image) attempts to predict the responses at the next lower level via feedback connections what propagates up is the prediction error signal, which is used to improve future predictions this is the predictive coding theory of perception
78
what is the role of the thalamus in visual processing?
the axons leaving the retinal ganglion cells go to the: - thalamus (specifically the lateral geniculate nucleus, which in turn projects to the primary visual cortex in the occipital lobe): visual information is processed in this pathway to determine what you are looking at - this pathway creates an internal (mental) representation of your entire visual space --> the objects in it, their position, and their attentional value - Midbrain (specifically the superior colliculi): visual information is used here to control fast visually-guided movements - the midbrain doesn't really know what you are looking at, but it knows where light is moving in visual space - Hypothalamus: visual information is used here to control circadian rhythms (such as sleep-wake cycles) - the hypothalamus doesn't know what you are looking at, but it knows how much light is present in your environment
79
What is the somatosensory system?
the somatosensory system provides information about touch, pressure, temperature, and pain on the surface of the skin and inside the body
80
what are the three interacting somatosensory systems?
the exteroceptive system (cutaneous/skin senses) responds to external stimuli applied to the skin (e.g., touch and temperature) the interceptive system (organic senses) provides information about conditions within the body and is responsible for efficient regulation of its internal milieu (e.g., heart rate, breathing, hunger, bladder) the proprioceptive (kinesthesia) system monitors information about the position of the body, posture, and movement (e.g., the tension of the muscles inside the body)
81
What are the different types of external stimuli that cutaneous senses encode?
the cutaneous senses (skin) encode different types of external stimuli: - pressure (touch) is caused by mechanical deformation of the skin - vibrations occur when we move our fingers across a rough surface - temperature is produced by objects that heat or cool the skin - pain can be caused by many different types of stimuli, but primarily tissue damage
82
What is the outermost layer of the skin called?
the outermost layer of skin is called epidermis ("above dermis") cells here get oxygen from the air (not the blood)
83
What is the middle layer of skin called?
the middle layer is called dermis
84
What is the deepest layer of skin called?
the deepest layer is called the hypodermis (or subcutaneous, "below the skin") sensory neurons are scattered throughout these layers (epidermis, dermis, hypodermis)
85
What is glabrous skin?
Glabrous skin is "hairless" skin (e.g., palms of hands and feet)
86
What do Merkel's disks respond to? (EPIDERMIS)
Local skin indentations (simple touch)
87
What are Ruffini corpuscles sensitive to? (DERMIS)
stretch and the kinesthetic sense of finger position and movement
88
What do Pacinian corpuscles respond to? (DERMIS)
skin vibrations
89
What do free nerve endings primarily respond to?
temperature and pain
90
Where are Meissner's corpuscles only found?
in glabrous skin they detect very light touch and localized edge contours (brail-like stimuli)
91
How does perception of temperature work?
There are two categories of thermal receptors: those that respond to warmth and those that respond to coolness - pain information is also conveyed by some of these cells this information is poorly localized, and the axons that carry it to the CNS are unmyelinated or thinly myelinated some of the receptor proteins that are sensitive to temperature can also be activated by certain ligands (e.g., capsaicin molecules activate heat receptors and menthol molecules activate cold receptors)
92
how does perception of pain work?
Sensations of pain and temperature are transduced by free nerve endings in the skin there are several types of pain receptor cells (usually referred to as nociceptors - "detectors of noxious stimuli") one type is the high-threshold mechanoreceptors (pressure receptor cells), which are free nerve endings that respond to intense pressure, like striking, stretching, or pinching other types of free nerve endings respond to extreme heat (or the presence of chemicals such as capsaicin, the active ingredient in chili peppers)
93
Axons from skin, muscles, and internal organs enter the CNS via spinal nerves. What are the 2 main pathways that they can take?
1. poorly localized information (e.g., crude touch, temperature, and pain) crosses over the midline in the spinal cord, just after the first synaptic connection - this information ascends to the thalamus through the spinothalamic tract 2. highly localized information (e..g, fine touch) ascends ipsilaterally through the dorsal column of the spinal cord - the first synapse in this pathway is in the medulla - from there, the information crosses over to the contralateral side as it ascends to the thalamus both pathways get bundled together in the midbrain before synapsing in the thalamus - from there, information goes to primary somatosensory cortex in the parietal lobe
94
What is the somatosensory homunculus?
When different sites of primary somatosensory cortex are electrically stimulated, patients report somatosensory sensations in specific parts of their bodies the relationship between cortical stimulations and body sensations is reflected in a somatotopic map of the body surface the somatotopic map is often referred to as the somatosensory homunculus ("little man")
95
What is tactile agnosia?
Patients with tactile agnosia have trouble identifying objects by touch alone when touching an object, people think this is that: - pine cone --> brush - ribbon --> rubber band - snail shell --> bottle cap however, these patients can often draw objects that they are touching, without looking, and they can sometimes identify objects from their drawings
96
What is phantom limb?
phantom limb is a form of pain sensation that occurs after a limb has been amputated amputees report that the missing limb still exists and that it often hurts one idea is that phantom limb sensation is due to confusion in the somatosensory cortices (primary and association) - the brain gets nonsense signals (in part from the cut axons) and it has difficulty interpreting them
97
What are the 6 different categories of taste receptors?
1. sweetness (molecules of sugar) - detected with a single metabotorpic receptor 2. umami (molecules of glutamate/glutamine) - detected with a single metabotropic receptor - the most common amino acid in animal products (meat and cheese) - MSG (monosodium glutamate) activates both salt and umami receptors 3. bitterness (a variety of molecules) - detected with 50 different metabotropic receptors that bind different bitter molecules 4. saltiness (positive ions such as sodium) - detected with an ion channel that is highly permeable to sodium 5. sourness (pH level; the concentration of free hydrogen ions) - detected with an ion channel that is highly permeable to free protons - cells that detect sourness are also responsible for the detection of astringency (e.g., the flavour of "salty licorice") and carbonation (bubbles), but the details are murky 6. fat (fatty acids) - detected with metabotropic receptors and fatty acid transporters
98
How does perception of gustatory information work?
transduction of taste is similar to chemical transmission that takes place at synapses when a tasted molecule binds to a taste receptor protein, it produces a change in membrane potential (either directly through an ion channel or through g protein signalling cascades) different tastes relate to the activation of different types of taste receptor proteins taste buds contain 20 to 50 taste receptor cells - each taste bud is dedicated to processing one type of taste (sugar, umami, bitter, salt, sour, or fat), which means that every cell within a taste bud expresses the same taste receptor protein taste receptor cells do not have traditional action potentials - they release neurotransmitter in a graded fashion taste receptor cells are replaced about every ten days, because they are directly exposed to a rather hostile environment to study the taste system, researchers often manipulate the DNA of mice - for example, to identify the sugar taste receptor, researchers remove specific genes from their genome and then test if mice can discriminate between regular water and sugar water researchers have even created mice where the sugar receptor gene was replaced with a bitter receptor gene - these genetically engineered mice cannot taste sugar, but they love the bitter molecule that now activates the cells in their sweet taste buds these studies demonstrate that much taste processing is innate (hard-wried from birth to be either pleasurable or aversive) sugar and umami taste receptor cells are instinctively rewarding/reinforcing - direct stimulation of them (or their downstream structures in the cerebral cortex) is inherently reinforcing - bitter taste receptor cells are instinctively aversive - animals can grow to appreciate some bitter taste cell activity, but it is an acquired taste interestingly, the entire cat family (including leopards, lions, tigers, cheetahs, jaguars, etc.) cannot taste sugar - they have evolved to only enjoy the savory, salty taste of meat
99
Where is the primary gustatory cortex located?
primary gustatory cortex is in the insular lobe of the cerebral cortex
100
How does the olfactory system work?
the olfactory system is specialized for identifying specific molecules called odorants the receptor proteins that transduce odorants into a change in membrane potential are metabotropic g protein-coupled receptors - each one is sensitive to a specific molecule odorant molecules are volatile substances that have a molecular weight in range of approximately 15 to 300 - most of them are lipid soluble and of organic origin, however many substances that meet these criteria have no odour
101
what is the olfactory epithelium?
the tissue of the nasal sinus that sits underneath the skull (the cribriform plate) and contains olfactory receptor cells - each olfactory cell expresses only one type of olfactory receptor protein
102
Where do olfactory receptor cells synapse?
in glomeruli in the olfactory bulb, which in turn sends axons into the brain
103
How many types of olfactory receptor cells does each glomerulus process information from?
just one (expressing a particular type of olfactory receptor protein) thus, each glomerulus processes a distinct odour
104
How can humans recognize up to ten thousand different odorants even though they only have ~400 different olfactory receptor protein/cell types?
through combinatorial processing
105
Are odours largely hard wired to be innately good or bad?
unlike taste, odours are largely not hard wired to be innately good or bad whether we like or dislike an odour is related to learned associations
106
Does olfactory information relay in the thalamus?
No, olfactory information does not relay in the thalamus it goes directly to primary olfactory cortex in the temporal lobe and the amygdala
107
What are pheromones?
Although most odours are not innately perceived as good or bad in young animals, pheromones are different pheromones are molecules released by one animal to signal something to another member of the same species - behavioural responses to pheromones are largely innate (hard-wired from birth) pheromones strongly influence the behaviour of many organisms, from prokaryotic cells to complex multicellular animals, but their existence in humans is controversial in many animals, especially insects, pheromones are used to: - attract or repel other members of the same species - signal attractiveness and sexual receptivity - mark a path to follow (as seen in ants) - signal danger
108
how does pheromone signalling work?
in mammals, the initial transduction and processing of pheromones occurs in the vomeronasal organ and "accessory olfactory bulb", which are next to but distinct from the regular olfactory epithelium and "main olfactory bulb" which process regular odours pheromones are detected by metabotropic vomeronasal receptors - these receptors are only distantly related to the olfactory receptors that detect normal odours, highlighting their different role humans, apes, and birds do not have funcitonal vomeronasal organs - they only have regular olfactory epithelium that detects normal odours (but it is certainly possible that some pheromone-like signalling occurs in this structure in humans)
109
How do pheromones affect rodent behaviour?
many mammals release pheromones in their urine - these molecules are usually not airborne - they must be actively sniffed or tasted to be detected rodents often sniff each other's genitals and each other's urine, and pheromone detection strongly influences their sexual behaviour female to male pheromone signalling is especially powerful - if the vomeronasal system is functional in a male mouse, they will only attempt to mate with female mice that are in heat - if the male vomeronasal system is damaged, they try to mate indiscriminately with any mouse, male or female male to female pheromone effects are more subtle - females prefer males that have healthy testosterone levels (vs. castrated males), presumably because of testosterone-induced male sex pheromone signalling
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what are some rodent male to female pheromone effects?
Lee-Boot effect - when female mice are housed together (without any male urine present), their estrous cycles slow down and eventually stop Whitten Effect - pheromones in the urine of male mice can trigger synchronous estrous cycles in groups of female mice Vandenbergh Effect - Earlier onset of puberty seen in female animals that are house with males Bruce Effect - the tendency for female rodents to terminate their pregnancies following exposure to the scent of an unfamiliar male THE URINE OF CASTRATED MALES DOES NOT PRODUCE THESE EFFECTS in general, rodent male to female pheromone effects are subtle and hard to reproduce - and human pheromone effects are notoriously hard to replicate - although several studies have found that females living in close proximity tend to have synchronized menstrual cycles, more recent work suggests that human menstrual synchrony does not exist
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What are soundwaves?
when an object vibrates, its movement causes the molecules of air surrounding it to alternately condense and rarefy (pull apart) these fluctuations in air pressure travel away from the source as a sound wave at approximately 700 miles per hour
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Under what conditions can the human ear transduce fluctuations in air pressure?
if the length of the sound wave is between 1.7cm and 17m this corresponds to sound waves that oscillate at frequencies between 20 and 20,000 times per second
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What are the 3 physical dimensions of sound?
LOUDNESS corresponds to the amplitude or intensity of the molecular vibrations - corresponds to the total number of hair cells that are active and their overall activity levels PITCH (tone) corresponds to the frequency of the molecular vibrations - it is measured in hertz (Hz) or cycles per second - moderate to high frequencies are encoded by place coding - low frequencies are partly encoded by rate coding TIMBRE corresponds to the complexity of the sound - we use timbre to help identify the source of the sound wave (through learning processes) - perceived by assessing the precise mixture of hair cells that are active throughout the entire cochlea
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Describe the anatomy of the ear
1. sound is funnelled through the PINNA (the outer ear) 2. Sounds coming down the ear canal cause the TYMPANIC MEMBRANE (the eardrum) to vibrate - these vibrations are transferred to the middle ear 3. the middle ear is comprised of three OSSICLES (small bones): the malleus, incus, and stapes - vibrations of the ossicles are transferred to the membrane behind the OVAL WINDOW - these vibrations are transmitted to the fluid-filled COCHLEA (the inner ear), which is a long coiled tube-like structure that contains sensory neurons
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What does the basilar membrane do?
the basilar membrane encodes high notes on the end closest to the oval window like a xylophone, the low notes correspond to the longest (widest) section
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Describe the cross section through the cochlea
the cochlea is divided into three longitudinal divisions: scala vestibuli, scala media, and scala tympani the receptive organ is the organ of Corti - it consists of the basilar membrane on the bottom, the tectorial membrane on the top, and auditory hair cells in the middle the cells that transduce sound are called hair cells because of their physical appearance - their hair-like extensions are called cilia outer hair cells have cilia that are physically attached to the rigid tectorial membrane - the cilia of inner hair cells are not attached to anything - they sway back and forth with the movement of the solution sound waves cause the basilar membrane to move relative to the tectorial membrane, which causes hair cell cilia to stretch and bend - the movement of the cilia pulls open ion channels, which changes the membrane potential of hair cells
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What are inner and outer hair cells?
although there are 3 times more outer hair cells than inner hair cells, only inner hair cells transmit auditory information to the brain outer hair cells contract like muscles to adjust the sensitivity of the tectorial membrane to vibrations - by regulating the flexibility of the tectorial membrane, outer hair cells influence the sensitivity of inner hair cells to specific frequencies of sound (i.e., different notes) people that do not have working inner hair cells are completely deaf - whereas people that do not have functional outer hair cells can hear, but not very well
118
Explain the working of hair cell cilia
the cilia of hair cells are connected to each other by TIP LINKS - elastic filaments that attach the tip of one cilium to the side of adjacent cilium the point of attachment of a tip link to a cilium is called an insertional plaque each insertional plaque has a single ion channel in it that opens and closes according to the amount of stretch exerted by the tip link
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What does loud noise do to hair cell cilia?
loud noises can easily break the tip links that interconnect each cilia - and hair cells cannot transmit auditory information without tip links fortunately, tip links usually grow back within a few hours - tip link breakage generally corresponds to temporary hearing loss (such as after a loud bang, or loud concert) tip link breakage is probably a protective measure, because too much glutamate release onto the cochlear nerve causes permanent cell death (excitotoxicity) 20% of 20-year-olds seem to have noise-induced hearing loss, presumably due to cochlear nerve damage
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How does perception of pitch work?
the major principle of auditory coding is that different frequencies of sound produce maximal stimulation of hair cells at different points on the basilar membrane this approach to encoding sensory information is known as PLACE CODING - the position of the most active hair cell in the cochlea indicates the fundamental frequency (the pitch) of the sound wave moderate to high frequencies are entirely encoded by place encoding - human speech is in this frequency range very low frequencies are largely encoded by RATE CODING
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What is Place Coding?
because of how the cochlea and basilar membrane are constructed, acoustic stimuli of different frequencies cause different amounts of movement along the basilar membrane - higher frequency sounds cause bending of the basilar membrane closest to the stapes, resulting in more hair cell activity in that area
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what is Rate Coding?
very low frequency sounds are processed using a rate coding system: the rate of neurotransmitter release from the hair cells deepest in the cochlea (furthest from the stapes) determines the perception of low frequency sounds
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What do V-shaped tuning curves tell us about sound?
Low points of three solid curves indicate that these inner hair cells will respond to faint sound only if it is of a specific frequency if the sound is louder, cells will respond to frequencies above and below their preferred frequencies lesions targeted to outer hair cells disrupt the responsiveness of inner hair cells to specific sounds
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What are overtones?
the fundamental frequency of a sound is the lowest frequency in the wave natural sounds are comprised of a fundamental frequency and a collection of overtones, which are generally integer multiples of the fundamental frequency - because strings (and membranes) are clamped on each end, oscillations tend to only occur at integer multiples of the fundamental frequency
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What is timber?
fundamental frequency - the lowest and most intense frequency of a complex sound - this frequency is what is most often perceived as sound's basic pitch overtone - sound wave frequencies that occurs at integer multiples of the fundamental frequency the timbre of sound refers to the specific mixture of frequencies (fundamental frequency plus overtones) that different instruments emit when the same note is played - it is the complexity of the sound wave - we analyze the timbre of a sound and how the timbre changes over time to identify which instrument made the sound
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How do cochlear implants work?
Typically, 20-24 electrodes are positioned along the length of the cochlea understanding human speech is often best when frequency positions corresponding to 250 Hz to 6500 Hz are stimulated the fundamental frequency of human speech is 85-180 Hz for men and 165-255 Hz for women, but the abundance of overtones can give the impression of the fundamental tone
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How does perception of spatial location work?
Phase differences and low-frequency sounds - we detect the source of continuous low-pitched sounds by means of phase differences - are the ears detecting compressed air at the same time? If so, the source must be equidistant from the two ears - the auditory system can identify phase differences of sound waves under 800 Hz, because these sound waves have a half wavelength that is larger than the dimension of the head Loudness and high-frequency sounds - we detect the source of high-pitched sounds by analyzing differences in loudness between ears - high frequency sounds are significantly dampened as they pass through our heads
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How does timbre relate to the perception of spatial location?
Sound waves bounce off the folds and ridges of the pinna (outer most part of ear) before entering the ear canal depending on the angle at which sound waves strike these folds and ridges, different frequencies of sound can be enhanced or attenuated (changing the timbre of the sound) animals can analyze how the timbre changes as they move their ears or head around - this helps them identify where the source of the sound is located for this to work, animals must first learn to recognize subtle changes in timbre when sound enters the ears from different angles
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How does auditory information go from the ear to the primary auditory cortex?
1. the organ of Corti sends auditory information to the brain via the cochlear nerve 2. these axons synapse in the cochlear nuclei of the medulla, where copies of the signal are made to be analyzed in parallel ascending paths 3. axons from the cochlear nuclei synapse in the superior olivary nuclei in the medulla and the inferior colliculi in the midbrain, both of which help localize the source of sounds 4. axons from the inferior colliculi synapse in the medial geniculate nucleus of the thalamus, which in turn relays the information to the... 5. Primary auditory cortex in the temporal lobe SONIC MG --> superior olivary nuclei --> inferior colliculi --> medial geniculate nucleus
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What is tonotopic representation?
like the basilar membrane, the primary auditory cortex is organized according to frequency - different parts of the auditory cortex respond best to different frequencies this organization, where different frequencies of sound are analyzed in different places of auditory cortex, is known as TONOTOPIC REPRESENTATION
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Describe the auditory cortex
primary auditory cortex (core region) is in the upper section of the temporal lobe, mostly hidden in the lateral fissure the belt and parabelt regions refer to auditory association cortex like visual information, auditory information is analyzed in "where" and "what" streams the posterior (dorsal) auditory pathway is involved in sound localization - this pathway meets up with the "where" vision pathway in the parietal cortex the anterior auditory pathway goes into the frontal lobe, where analysis of complex sounds occur (the "what" are you hearing pathway)
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What is auditory agnosia?
music and language are special, complex forms of auditory processing, and brain damage in auditory association cortex can cause very specific types of auditory agnosia Different areas of auditory association cortex process the melody, rhythm, and harmony (overtones) of music other areas of auditory association cortex are involved in the perception of sound as pleasant (consonant) or unpleasant (dissonant), and certain combinations of musical notes can trigger emotions (happy or sad) accordingly, there are many different types of auditory agnosias
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What is amusia?
Amusia is the inability to perceive or produce melodic music - people with amusia might be unable to sing or recognize the happy birther song people with amusia can often converse and understand speech - they can also recognize environmental sounds they can even recognize the emotions conveyed in music, but they will typically be unable to tell the difference between consonant music (pleasant sounding harmony) and dissonant music (unstable, transitional), even though these sounds might alter their emotional state just as they do in other people
133
What is the vestibular system and how does it differ from the cochlea?
Vestibular system: detects gravity and angular acceleration of the head cochlea: detects sound the vestibular system does not produce any readily definable, conscious sensation - instead, it maintains your upright head position, organizes your balance, and corrects eye movements to compensate for head movements
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What are semicircular canals?
three ring-like, fluid-filled structures that detect changes in head rotation (angular acceleration)
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What are vestibular sacs?
a set of two receptor organs in each inner ear (utricle and saccule) that detect changes in the tilt of head (gravity) the utricle and saccule in the vestibular sac respond to the force of gravity and inform the brain about the head's orientation
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What is the cupula?
gelatinous mass found in the ampulla of the semicircular canals; moves in response to the flow of fluid in canals
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How do we measure brain activity?
by attaching electrodes to the scalp to record an electroencephalogram (EEG)
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How do we measure muscle activity?
by attaching electrodes to the chin to record an electromyogram (EMG)
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How do we measure eye movement?
electrodes are also placed near the eyes to measure eye movements via an electro-oculogram (EOG)
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Explain the EEG signals during sleep
BETA ACTIVITY - 12-30 Hz - typical of an aroused state - it reflects desynchronous neural activity (high frequency, low amplitude oscillations) ALPHA ACTIVITY - 8-12 Hz - typical of awake person in a state of relaxation THETA ACTIVITY - 4-8 Hz - appears intermittently when people are drowsy, and is prominent during early stages of sleep DELTA ACTIVITY - <4 Hz - occurs during deepest stages of slow-wave sleep reflects synchronized low frequency, large amplitude brain activity
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What is rapid eye movement (REM) sleep associated with?
also called paradoxical sleep is associated with desynchronized EEG activity, rapid eye movements, dreaming, and muscle paralysis; muscles are totally inactive apart from occasional twitches cerebral blood flow and oxygen consumption INCREASE
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Describe EEG during deep sleep
Slow-wave sleep - stage 3/4 non-REM sleep (also known as deep sleep) - corresponds to large amplitude, low frequency oscillations of brain activity as measured with EEG - this pattern of neural activity reflects synchronized bursts of action potentials in large collections of neurons
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What are the findings of REM deprivation studies?
animals can sleep sitting or standing up, but muscles go limp during REM sleep when this happens, animals fall off the pedestal and into the water
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how does lack of sleep cause death?
in an apparatus, an experimental rat is kept awake because the onset of sleep (detected with EEG) triggers movement of the cage floor the control rat can thus sleep intermittently, whereas the experimental animal cannot after two to three weeks of sleep deprivation, the experimental animals begin to lose control of their metabolic processes and body temperature soon they lose weight and die
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Why is sleep critical for survival?
if you don't sleep... - you feel tired, but generally, physically, your body is fine - your mind however begins to deteriorate - you start to exhibit delayed reaction times and poor judgment (as measure on performance in cognitive tests) - you have increases in stress hormones, mood swings, and impulsive behaviour - you exhibit worse learning and memory - you increase your propensity for weight gain, migraines, hallucinations, dementia, seizures, and death - a sleep debt is created that must be repaid (in most species) to some extent - microscleep states often appear, where animals fall asleep for brief episodes lasting several seconds, during which time they are perceptually "blind" and often unaware that they have fallen asleep - sleep disruption often precede and exacerbate mental illnesses
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What is so special about dolphin sleep?
dolphin sleep highlights an especially remarkable solution to the problem of maintaining vigilance during sleep their version of sleep alternates between the two cerebral hemispheres
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How much of human infant sleep is REM sleep?
50%
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How much of human adult sleep is REM sleep?
25%
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What are some differences in sleep between species?
amount of sleep ratio of REM to non-REM sleep Length of sleep cycles (average time between two REM events) as a general rule, predatory animals indulge in long, uninterrupted periods of sleep animals that are preyed upon typically sleep during short intervals that may last no more than a few minutes
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What is the correlation between sleep and body weight?
the amount of time a species sleeps each day is inversely correlated with weight
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What is the correlation between metabolic rate and body weight?
while overall metabolic rate increases as mass increases, metabolic rate per pound (or per cell) decreases as mass increases
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what is the correlation between metabolic rate and sleep?
higher body mass, higher brain mass, higher overall metabolic rate but lower metabolic rate per kg (or per cell), lower heart rate, longer life span, lower total sleep time, longer length of sleep cycles example: large animals have low metabolic rates per cell and long life spans - they don't sleep very much, but each sleep session is relatively long
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Why do all this correlations with sleep exist?
one hypothesis is that it all has to do with economies of scale related to heat savings and nutrient/waste distribution networks - large animals benefit from economies of scale (i.e., heat savings and more efficient distribution networks), so each cell doesn't have to work as hard as it does in a small animal the fact that total sleep time is highly correlated with all of these variables suggests that sleep may be critical for a restorative process
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What are the main theories as to why animals sleep?
1. To recover from physical or mental exertion - if the function of sleep is to recover from physical or mental exertion, then the amount of time spent exercising and thinking should correlate with total sleep time - the amount of sleep people get does not correlate very well with how much or how little they exercise or study - people who suddenly start exercising a lot (or suddenly get confined to a wheelchair) do not tend to sleep any more or less than normal - there is a reduction in blood pressure and heart rate when people sleep (especially during deep sleep), but the caloric difference between a person sleeping and sitting across 8 hours is negligible (~110 calories) 2. Brain processing (learning and memory) - How can the brain update synaptic weights while it is currently operational and constantly receiving new information? - sleep gives the brain an opportunity to reorganize data and archive memories, which perhaps cannot be done efficiently while awake - synaptic modifications clearly occur during sleep - learning and memory are clearly impacted by sleep - the amount of slow-wave and REM sleep people get correlates with improvements in declarative and procedural memory, respectively - during sleep the brain appears to be actively processing information and transferring it between different areas, both within cells (with gene transcription) and between cells (through network oscillations) 3. Waste removal - since total sleep time correlates with body size (as well as brain size, metabolic rate, heart rate, and life span), maybe it is critical for a process that benefits from economies of scale, such as nutrient use or waste removal - some evidence suggests sleep is required for efficient removal of waste products from the brain - the concentration of many proteins in the brain increases across periods of wakefulness and decreases across periods of sleep - it seem that the clearance of proteins and waste products from the brain is almost non-existent during wakefulness but really high during sleep
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How does waste removal happen during sleep?
when animals sleep, glial cells in the brain (astrocytes) seem to lose water and shrink in size - this increases the total volume of interstitial space (i.e., extracellular solution), which promotes diffusion of cerebrospinal fluid through the brain, clearing away waste accordingly, big animals may sleep less than small animals because waste clearance systems in the brain benefit from economies of scale - larger brains seem to have more space to accumulate garbage and they can clear away waste faster than smaller brains
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What is the glymphatic system?
cerebrospinal fluid (CSF) is a clear, colorless fluid that is continually being made in brain ventricles - CSF circulates around the brain and diffuses into it, into the interstitial space, thus becoming the extracellular solution that surrounds neurons - as CSF moves through the interstitial space, it clears waste products away before exiting into blood vessels this process is known as the glymphatic system (in contrast to the lymphatic system, which clears away cellular waste everywhere else in the body) - the glymphatic system removes excess proteins and other waste from the interstitial space of the brain the clearance of waste from the brain may be minimal during waking hours but high during sleep
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Why didn't animals just evolve bigger brains so CSF can diffuse around the brain and clear away waste all the time?
nobody knows, but almost all signalling molecules in the brain act via diffusion, and constraining diffusion is a prominent aspect of regulatory control there may have been evolutionary pressure to control and constrain diffusion within the brain to such an extent that waste products can now not be effectively cleared while the brain is functioning thus, sleep may have evolved to let the brain perform optimally most of the day
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What are circadian rhythms?
the daily change in behaviour and physiological processes that follows a cycle of approximately 24 hours is known as a circadian rhythm circadian rhythms are controlled by internal biological clocks - regular daily variation in light levels keeps the clock adjusted to 24 hours rats are normally active at night - if we shift the cycle by a couple hours, the rat's activity cycle changes as well - the body adapts to this change if the light is constantly dim, the rat finds its own source of rhythmicity (due to an internal biological clock) - they will maintain their circadian rhythms to a large extent, but these rhythms will drift over time (23 or 25 hour cycles) - a brief period of bright light will reset their internal clock
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What is the role of the suprachiasmatic nucleus (SCN)?
the suprachiasmatic nucleus (SCN) of the hypothalamus regulates sleep-cycle cycles - it receives a direct input from the retina lesioning the SCN dramatically alters circadian rhythms (such as sleep-wake cycles and hormone secretions) SCN lesions alter the length and timing of sleep-wake cycles, but they do not change the total amount of time that animals animals spend asleep
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What makes the clock of SCN neurons "tick"?
circadian rhythms are maintained by the production of several genes and two interlocking feedback loops - basically, when expression of one protein gets high enough, it inhibits its own production and promotes the expression of a different protein advanced sleep phase syndrome - a mutation of a gene called per2 (period 2) causes a 4-hour advance in the biological clock (rhythms of sleep and temperature cycles) - a strong desire to fall asleep at 7pm and wake up at 4am delayed sleep phase syndrome - a mutation of a gene called per3 causes a 4-hour delay in rhythms of sleep and temperature cycles - a strong desire to fall asleep at 2am and wake up at 11am
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What is the sleep molecule hypothesis?
while the SCN maintains the body's master clock, what determines how much an animal needs to sleep? SCN lesions do not change total sleep time consistent with the waste removal theory of sleep, there is a build up of many molecules in the interstitial fluid of the brain during waking hours - these molecules are generally cleared away during sleep - some of these molecules promote drowsiness and sleep at high concentrations the adenosine molecule (part of ATP) has received lots of attention - adenosine levels rise in the brain during waking hours and accumulate even more with sleep deprivation - adenosine levels fall rapidly in the brain during sleep, even during brief intrusions of sleep drowsiness and the duration and depth of sleep are strongly modulated by adenosine receptor signalling throughout the brain caffeine, which promotes arousal, is an adenosine receptor antagonist adenosine is likely one of many sleep-inducing molecules in the brain - it is likely the build-up of these molecules during waking hours that underlies animals' homeostatic need for sleep
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What are the signalling molecules that are released by neurons that show increased activity during periods of arousal, alertness, and wakefulness and decreased activity during slow-wave sleep?
serotonin (raphe nuclei in hte hindbrain) norepinephrine (locus coeruleus in the hind brain) acetylcholine (throughout the brain) orexin (hypothalamus) histamine (hypothalamus) orexin and histamine are neuropeptides that are released by neurons in the hypothalamus - histamine receptor blockers (antihistamines) often cause drowsiness
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What is the correlation between focus/attention and norepinephrine neuron activity?
norepinephrine neuron activity tends to positively correlate with focus and attention
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What is the correlation between serotonin (5-HT) neuron activity and cortical arousal and drugs that increase serotonin signalling?
serotonin (5-HT) neuron activity positively correlates with cortical arousal (as measured by EEG), and drugs that increase serotonin signalling tend to suppress aspects of REM sleep (without affecting memory)
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Describe the sleep/wake flip-flop circuit
Neurons in the ventral lateral preoptic area (vlPOA) of the hypothalamus promote sleep - electrical stimulation of this area causes drowsiness and sometimes immediate sleep - lesions suppress sleep and cause insomnia - vlPOA neurons inhibit wake-promoting neurons - but this area receives inhibitory inputs from the same regions it inhibits - this kind of reciprocal inhibition characterizes a flip-flop circuit; both regions cannot be active at the same time and the switch from one state to another is fast the animal is awake when the arousal, wake-promoting system is more active than the vlPOA neurons - the animal is asleep when vlPOA neurons are more active than the wake-promoting arousal system
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What is the adenosine version of the sleep molecule hypothesis?
there are adenosine receptors on many neurons throughout the brain extracellular adenosine builds-up during the day sleep-promoting vlPOA neurons are activated by adenosine signalling - arousal-promoting acetylcholine (ACh) neurons are inhibited by adenosine signalling the influence of adenosine signalling during the day can be masked by other regulators of sleep and arousal, such as SCN neuron activity but at some point, when the clock of SCN neurons aligns with the build-up (or clearance) of sleep-promoting molecules, the whole network flip-flops and the animal transitions into (or out of) sleep
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What is orexin?
also known as hypocretin is a peptide produced by neurons in the lateral hypothalamus (LH) - orexin neuron activity promotes wakefulness - motivation to remain awake activates orexin neurons most forms of narcolepsy are associated with the absence of orexin neurons
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What is narcolepsy?
a rare sleep disorder characterized by periods of excessive daytime sleepiness and irresistible urges to sleep the disease is related to the death of orexin neurons in the hypothalamus - they seem to be attacked by the person's own immune system, usually during adolescence or young adulthood other symptoms include: - sleep paralysis - when REM-associated paralysis occurs just before a person falls asleep or just after they wake up - it is often accompanied by vivid, dream-like hallucinations - cataplexy - when complete muscle paralysis suddenly occurs when someone is awake - it is typically precipitated by strong emotional reactions or sudden physical effort (e.g., laughter, anger, excitability)
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What is insomnia?
insomnia is characterized as difficulty falling asleep after going to bed or after awakening during the night insomnia is a problem that affects approximately 25% of population occasionally and 9% regularly FATAL FAMILIAL INSOMNIA & SPORADIC FATAL INSOMNIA - a very rare disease that involves progressively worsening insomnia, which leads to hallucinations, delirium, confusional states, and eventually death (within a few years) - it is typically associated with progressive neurodegeneration around the thalamus, hypothalamus, and/or brain stem
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What are some disorders associated with non-REM sleep (non-REM parasomnias)?
there are many sleep disorders that occur during non-REM sleep or during transitions out of sleep - they are called non-REM parasomnias - the brain seems to get caught in between a sleeping and waking state - many people are unaware they exhibit this behaviour Sleepwalking, sleep-talking, sleep-groaning, sleep-crying, sleep-eating, sleep-masturbating, sleep-teeth grinding - some of these conditions tend to be more prevalent in children (i.e., people can grow out of it) - episodes can last seconds to minutes or longer - these states can be caused by certain medications or medical conditions Sleep terrors - characterized by overwhelming feelings of terror upon waking - may include panic and screaming and bodily harm caused by rash actions - people sometimes have no recollection of these events - prevalent in people diagnosed with PTSD
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What is REM sleep behaviour disorder?
neurological disorder in which the person does not become paralyzed during REM sleep and thus acts out dreams appears to be a neurodegenerative disorder with at least some genetic component it is often associated with more common neurodegenerative disorders such as Parkinson's disease
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What is sexual dimorphism?
sexual dimorphism is the condition where the two sexes of the same species exhibit different characteristics beyond the differences in their sexual organs these differences may be subtle or exaggerated and can include differences in size, weight, colour, behaviour and cognition - they include secondary sex characteristics (i.e., features that occur during puberty) sexual dimorphism is associated with genetic and hormonal differences both before and after birth
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What are sexual dimorphic behaviour?
sexual dimorphic behaviours are behaviours that take different forms, or occur with different probabilities, or under different circumstances across males and females of the same species in mammals, the most striking category of sexual dimorphic behaviours are reproductive behaviours, including courting, mating, parenting, and most forms of aggression the brain gives rise to sexual dimorphic behaviours because it is a sexually dimorphic organ - the size and interconnectivity of different brain regions vary according to sex in terms of human behaviour, there are differences between the sexes, on average, in their mixture of talents, temperaments, and interests these differences can be the result of biology, socialization, and the interaction of the two
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how is sex defined?
sex is defined at birth by the presence of particular sex chromosomes, sex hormones, and sex organs
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what does gender refer to?
gender refers to the range of characteristics that pertain to, and differentiate between, masculinity and femininity, which are the characteristics associated with men and women, respectively - these characteristics reflect biology and culture
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What is gender expression?
it it the expression of masculinity and femininity
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what are gender roles?
they refer to the behaviours and attitudes that are deemed typical, appropriate, or desirable for people of a given sex
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what does sexual behaviour refer to?
refers to the actual sex acts performed by the individual
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what is sexual orientation?
refers to one's enduring romantic or sexual attractions
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What is sexual identity?
refers to an individual's conception of themselves in terms of whether they identify (or not) with a sexual orientation
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What is gender identity?
it is one's personal sense of their gender - it is usually but not always consistent with masculine and feminine body development
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Why is gender a social construct?
the consensual rules for determining gender (and race) designations differ across time and across cultures in a manner that is independent of changes in biology this evidence that our understanding and categorization of masculinity and femininity are socially constructed from our shared experiences biology influences these social constructions, but its contributions are not decisive - how large or small the biological contributions are depend on contemporaneous cultural influences our brains and our behaviours (as well as our conceptions of them) are complex outcomes of both biological and cultural influences
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What is the problem with determining the differences between the sexes?
"There are ___ differences between the brains of males and females" "There are ___ differences in the behaviour of men and women" this kind of statement is typically an opinion about the relative influence of innate biology versus culture on gender expression (masculinity and femininity) the problem is that the strength of the culture determines the strength of the biological influences confusingly, biological differneces are most influential in cultures where everyone is treated the same and gender isn't taught - in contrast, cultures with strong and specific ideas about gender tend to mask the complexity and variability of the biology - thus, arguments about the size and importance of innate sex differences are generally opinions about the how strong the cultural influences should be and not about the extent that biological differences should be respected
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How does socialization influence behaviour?
when socializing children, sometimes we support whatever behaviours spontaneously emerge - more commonly, we pre-emptively encourage/discourage certain behaviours to ensure their expression is congruent with our values and the dominant culture these days, there are strong disagreements about whether (and how much) certain expressions of gender are toxic, good, or innocuous how does the study of biology help resolve these arguments? things that are innate, natural, or biological are not inherently good or bad - the value of these things is determined by people based on their culture Note: general intelligence (or even aptitude to perform any particular job) is not located in a single neuroanatomical structure - traits like general intelligence are hard to define, let alone measure, and we know that very different brains can produce similar levels of intellectual performance
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What are gametes?
gametes are mature reproductive cells made by gonads (ovaries or testes) - they are either ova (egg cells) or sperm unlike all other cells in your body, which typically have 23 pairs of chromosomes (23 from your biological mother and 23 from your biological father), gametes only have one copy of each chromosome (a mix from your mother and father) one pair of chromosomes are called the sex chromosomes, as they usually determine the organism's sex - they come in X and Y varieties
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what are the 5 factors present at birth that are used to determine an animal's biological sex?
sex chromosomes: XX or XY gonads: testes or ovaries sex hormones; androgen signalling internal reproductive anatomy external anatomy generally, the five factors are either all male or all female - atypical combinations give rise to intersex conditions, in which the person cannot be distinctly identified as male or female
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What are the three categories of sex organs?
gonads (testes or ovaries) internal reproductive anatomy external anatomy
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TRUE or FALSE: Not all embryos contain precursors for both female and male sex organs?
FALSE all embryos contain precursors for both female and male sex organs
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What are undifferentiated gonads?
embryonic precursor of ovaries/testes
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What is the the Müllerian system?
embryonic precursors of female internal sex organs
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What is the Wolffian system?
ebryonic precursors of male internal sex organs
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What happens during the second month of gestation?
the undifferentiated gonads typically develop into ovaries or testes
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What happens during the third month of gestation?
typically either the Müllerian or Wolffian system develops while the other withers away
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Describe the male sex organ development
the SRY gene that is normally located on the Y chromosome encodes a protein that causes undifferentiated fetal gonads to develop into testes SRY gene --> development of testes --> embryonic release of: - anti-Müllerian hormone --> stops development of Müllerian system (internal female sex organs) - androgens (testosterone) --> triggers development of male sex organs (both internal and external)
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what is the defeminizing effect?
effect of anti-Müllerian hormone early in development, which PREVENTS development of the female-typical internal anatomy
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What is the masculinizing effect?
effect of androgen hormones early in development, which TRIGGERS development of male-typical anatomy
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What are androgens?
male sex hormones testosterone is the principal mammalian androgen - it is released by the testes, and it triggers development of the Wolffian system (internal male sex anatomy) some testosterone is converted into dihydrotestosterone, which is what triggers development of external male sex anatomy
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Describe female sex organ development
XX chromosome (if you do not have two X chromosomes, you will not have ovaries) --> development of ovaries --> which are largely silent until puberty - puberty is triggered by hormones released from gonads (ovaries or testes) - the ovaries do not release any critical signalling molecules before puberty - so, what triggers development of female reproductive anatomy? in the absence of anti-Müllerian signalling, the Müllerian system develops into internal female reproductive anatomy, which includes the inner vagina, uterus, and fallopian tubes in the absence of testosterone signalling, external female sex organs (vulva) develop while the Wolffian (male internal) system withers away
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What happens when you don't have either the SRY gene (development of gonads into testes) or two XX chromosomes (development of gonads into ovaries)?
- Turner Syndrome (X0) is when you only have one sex chromosome - associated with other developmental abnormalities on account of missing a full chromosome - Swyer Syndrome (XY) is when you are XY but have a bad SRY gene In both cases, gonads do not develop (neither testes nor ovaries), but female-typical sex organs develop normally - people without gonads are infertile - they also do not naturally experience puberty, but that is easy to artificially induce with hormone injections it is possible to have two (or more) X chromosomes as well as the SRY gene (e.g., XXY or XXXY) - this is usually results in typical male development patterns (but also infertility)
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What if the production of anti-Müllerian hormone is insufficient or the receptors for it are lacking in either number or function? (for a person who has healthy XY chromosomes (male) and their SRY gene successfully triggers testes development)
insufficient anti-Müllerian hormone signalling will cause insufficient anatomical defeminization: both male and female internal sex organs will develop and get tangled together - there is often functional external male genitalia
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What if theres is insufficient androgen signalling? (for a person who has healthy XY chromosomes (male) and their SRY gene successfully triggers testes development)
androgen insensitivity syndrome results in anatomical defeminization with partial or no masculinization in severe cases, no internal sex organs develop - in these cases, people typically develop normal external female genitalia and identify as heterosexual women, but they will be infertile and have a short vagina in mild cases, the external genitalia is fully masculinized intermediate cases are associated with ambiguous external genitalia
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What are organizational effects of sex hormones?
sex hormones influence the development of the body and brain - these effects are permanent and put you on a particular trajectory going forward behavioural defeminization - refers to organizational effect of androgens on the brain that prevent animals from displaying female-typical behaviours in adulthood behavioural masculinization - refers to organizational effect of androgens on the brain that enables animals to engage in male-typical behaviours in adulthood
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What are activational effects of sex hormones?
puberty causes sex hormones to be released by the gonads, which influence both body and mind the production of sperm, ovulation, and general horniness are all examples of activational effects how the mind and body respond to activational hormone signalling in adulthood depends on how the body and brain were organized by hormone signalling in utero
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what is kisspeptin?
neuropeptide produced by neurons in the hypothalamus that initiates puberty and maintains reproductive ability by triggering release of gonadotropin-releasing hormone
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what is gonadotropin-releasing hormone?
Hypothalamic hormone that stimulates anterior pituitary gland to secrete gonadotropic hormones
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What are gonadotropic hormones?
hormones of pituitary gland (follicle-stimulating hormone, FSH, and luteinizing hormone, LH) that have stimulating effect on cells of gonads
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Explain male sexual behaviour
human males are like other male mammals in their behavioural responsiveness to testosterone with normal levels of testosterone, males can be fertile; without testosterone sperm production ceases, and sooner or later, so does the ability to have sex a castrated male rat will cease sexual activity, but it can be reinstated with an injection of testosterone men taking a gonadotropin-releasing hormone antagonist will not show testicular release of androgens and have a decrease in sexual interest and intercourse
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What is estrogen?
class of sex hormones released by the ovaries that cause maturation of the physical features and characteristic of females, such as growth of breast tissue and female genitalia
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What is estradiol?
principle estrogen of many mammals, including humans
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What controls both the menstrual and estrous cycles?
both menstrual and estrous cycles are controlled by the two ovarian hormones estradiol and progesterone
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describe the menstrual cycle
female reproductive cycle of most primate, including humans characterized by menstruation (if pregnancy does not occur), concealed ovulation, and the absence of a mating season sexual arousal is somewhat influenced by ovarian hormones, but ability to mate is not - animals with a menstrual cycle exhibit sexual activity throughout the cycle
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describe the estrous cycle
female reproductive cycle of most mammals (other than most primates) females that have estrous cycles do not menstruate; they absorb their endometrium - they also display clear outward signs of ovulation and fertility they are typically only sexually active during the estrous phase of their cycle, which is referred to as being "in heat" - this change in physiology and behaviour alters the behaviour of nearby males
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Expain the hormonal control of sexual behaviour
the organizational effects of hormones on the body (i.e., sex organs) is largely over by birth - however, the organizational effects of hormones on the brain continues for a few weeks after birth, at least in rodents One consequence of this is that we can masculinize or feminize the brain of rodents by altering hormone signalling immediately after birth, after the anatomical development of their sex organs is complete for example, when male rodents are castrated at birth (which stops further androgen signalling), they develop some female-typical behaviours - if they are injected with female sex hormones in adulthood (estradiol and progesterone), they will try to get other males to have sex with them (i.e., they will assume lordosis in the presence of other males) injections of female sex hormones in non-castrated male rats (or males castrated in adulthood) have relatively small behavioural consequences, at least following single injections
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What do human adrenal glands for hormonal control of sexual behaviour?
Human adrenal glands, which are present in men and women, typically secrete a small amount of androgens - however, some people's adrenal glands secrete abnormally large amounts of androgens, which can start either before or after birth
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What does excess androgen signalling do in human males and females?
in males, excess androgen signalling from adrenal glands has minimal effect, since thier testes already secrete tons of androgens in females, excess androgen signalling can cause some degree of masculinization of either the body or brain or both - if the condition is present at birth, it is congenital adrenal hyperplasia (CAH)
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what can cause an enlarged clitoris and partially fused labia?
depending on the amount of androgen signalling during development, sex organs can become slightly masculinized brain anatomy and function can also be masculinized females with CAH have a higher likelihood of identifying as a man and being sexually attracted to women in comparison to other females the implications of this research are that sexual orientation and gender identity might be determined by the timing and effectiveness of androgen signalling in the brain during early development
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How did researchers identify the important neural pathways in female sexual behaviour neural circuitry?
by injecting transneuronal retrograde tracer in muscles responsible for lordosis response in female rats, researcher identified the important neural pathways: VMH --> PAG --> nPGI --> motor neurons in spinal cord
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what is the periaqueductal gray matter? (in female seuxal behaviour neural circuitry)
the destruction of it abolishes sexual behaviour estradiol treatment or stimulation of VMH increases neural activity neurons contain estrogen and progesterone receptors
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What is the medial amygdala? (in the female sexual behaviour neural circuitry)
mating cause production of Fos protein neurons contain estrogen and progesterone receptors
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What is the ventromedial nucleus of hypothalamus (VMH)? (in the female sexual behaviour neural circuitry)
large nucleus in the hypothalamus that plays an essential role in female sexual behaviour in rodents: - electrical stimulation of VMH facilitates female sexual behaviour - injections of estradiol and progesterone directly into VMH also stimulates sexual behaviour, even in females whose ovaries have been removed - female with bilateral lesions of VMH will not display lordosis, even if she is treated with estradiol and progesterone mating causes production of Fos protein neurons contain estrogen and progesterone receptors
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what is the important pathways for male sexual behaviour?
mPOA --> PAG --> nPGI --> motor neurons in spinal cord
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What is the medial preoptic area (mPOA)?
nucleus in the anterior hypothalamus that plays essential role in male sexual behaviour - electrical stimulation of mPOA in rodents elcitis male copulatory behaviour - within the mPOA, there is an area called the sexually dimorphic nucleus (SDN) of preoptic area - this nucleus is much larger in males than in females - lesioning the mPOA of female rats does not affect their sexual behaviour, but it does cause them to ignore their offspring
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How does formation of long-lasting, monogamous-ish pair bonds happen?
in approximately 5% of mammalian species, sexually mature couples tend to form long-lasting, fairly monogamous pair bonds - some species of prairie voles form long-term pair bonds - some don't the formation of pair bonds seems to relate to two peptides in brain: VASOPRESSIN and OXYTOCIN - these compounds are released as neuropeptides in the brain and as hormones in the blood - levels of them are elevated during sex, childbirth, and breastfeeding the prairie vole species that form long term pair bonds have more vasopressin and oxytocin receptors in their ventral forebrain than other species do - pharmacologically blocking or activating these receptors influences who they pair up with and when artificially increasing the expression of these receptors in non-monogamous prairie vole brains causes them to form life-long, monogamous-ish pair bonds
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what does regulating our priorities do for us? (falling in love or becoming a drug addict?)
to ensure that we attain critical biological goals (e.g., survival, reproduction), specific brain circuits determine how valuable things are to us unlike memorizing your numbers and letters, deep emotional learning completely alters what matters to you - love and addiction do not affect overall intelligence; they skew priorities and choice behaviour "I felt as though I couldn't survive without it" - if you beleive that something silly is essential to your survival, your priorities won't make sense to others - people with an addiction can push through negative experiences because they feel as though they can't survive without that thing, substance, or person getting over a devastating breakup is somewhat like recovering from addiction - healing a broken heart is difficult and often involves relapses into obsessive behaviour the brain areas that mediate these decisions and set priorities regulate our motivational processes and feelings of pleasure and happiness
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What does the range of our emotions relate to?
our capacity to conceptualize, categorize, label, interpret, and introspect about our outer and inner worlds animals, lacking our language and culture, likely do not experience the world the same way we do
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how do many species of animals broadcast their emotions?
with postural changes, facial expressions, and nonverbal sounds (such as sighs, moans, and growls) facial expressions of emotion are minimal when people are by themselves
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How many difference classes of facial expressions can people reliably discriminate and what are they?
between six different classes of facial expression: fear, anger, surprise, disgusted, sad, and happy
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How quick can recognizing the emotions of others through their facial expressions happen?
recognizing the emotions of others through their facial expressions is generally automatic, rapid, and fairly accurate when people are given more time to think about the emotion conveyed by facial expressions, they tend to show very little improvement
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what do faces offer us in terms of serving a social function?
emotional expressions serve a social function faces offer a rich, salient source of information for navigating the social world - they play a role in deciding whom to love, whom to trust, whom to help, and who is found guilty of a crime
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How do we know that facial expressions are innate?
facial expressions are innate, natural ,unlearned responses involving complex muscles movements the ability to display emotions and recognize them in others transcends cultural and linguistic barriers (to some extent) babies as young as 36 hours display (mimic) universal facial expressions there are no differences in the display of emotional facial expressions between congenitally blind, non-congenitally blind, and sighted athletes an isolated tribe in New Guinea had no trouble recognizing emotional expressions in Westerners, and Westerners had no trouble recognizing emotional expressions in them
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what is an issue with solely relying on facial expressions to go about knowing how someone is feeling?
emotional facial expressions are not super specific - the same facial expression can convey different emotions and different facial expressions can convey the same emotion inferring emotions from facial expressions is not very reliable - the same emotion is not reliably expressed through nor perceived from a common set of facial movements the generalizability (contextual and cultural effects) of deducing emotions from facial expressions is not well studied overall, emotional experiences do not reduce to six different types of emotions - there seems to be about 25 unique emotional blends, and they do not manifest in prototypical facial-muscles configurations alone, but rather in multimodal behavioural expression involving voice, touch, posture, gaze, and head/body movements
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what does it mean for emotions to exist in the abstract?
you can cognitively think about emotions and make your face artificially express specific emotions (like when people tell you to smile to look happy or you pretend to be sad) - this aspect of emotions is processed in the neocortex emotions also exist as a feeling, a raw reflexive response to certain stimuli - this aspect of emotions is processed in the limbic system, most prominently in the amygdala
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what are the different pathways that sensory input diverges into?
a stream of THOUGHT and a stream of FEELING the stream of thought is processed in the neocortex the stream of feeling is processed in the limbic system
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why do actors often try to experience real emotions on set, rather than trying to fake them?
genuine facial expressions tend to be automatic and involuntary they sometimes even involve different facial muscles than artificial expressions of emotions
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What is volitional facial paresis?
it is a condition where people are unable to voluntarily control their facial muscles, but they can express genuine emotion, even using the same muscles caused by damage to face region of primary motor cortex or its subcortical connections
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what is emotional facial paresis?
the reverse of volitional facial paresis lack of movement of facial muscles in response to emotions in people who have no difficulty moving these muscles voluntarily caused by damage around insular cortex or parts of the thalamus
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What are behavioural responses?
they consist of muscular movements (facial expressions, body language, choreographed movements)
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what are autonomic responses?
they signal through peripheral nervous system they facilitate fight or flight behaviours and provide quick mobilization of energy for vigorous movement
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What are hormonal responses?
they signal through blood reinforce the autonomic responses
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What is the common-sense view version of the theory of emotion?
1. perception of the emotion-eliciting event (e.g., see a bear) 2. subjective feelings of emotion (e.g., fear) 3. behavioural and physiological responses (e.g., trembling, sweating, and running away) the common-sense view is that the subjective feelings of emotion precede and cause the associated physiological response
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What is James-Lange's theory of emotion?
1. perception of emotion-eliciting event (e.g., see a bear) 2. appropriate set of behavioural and physiological responses are triggered (e.g., clench fists, run away, sweating, trembling, increased heart rate) 3. The brain receives feedback form these changes in the peripheral nervous system which, in turn, produces the subjective feeling of emotion (e.g., fear) the James-Lange theory was ased on studies of people with spinal cord injuries at different levels in the late 1800s - people with spinal cord damage reported feeling less intense emotions - the reduction in emotional experiences correlated with how much sensation the people had lost (how paralyzed they were, the height of the spinal cord damage) - some subjects looked and acted angry at times, but they reported that they did not feel very angry interfering with the muscular movement associated with a particular emotion slightly decreases people's ability to experience that emotion - this has been reported following Botox injections into the face to reduce wrinkles However - our internal organs are relatively insensitive and do not respond quickly enough to account for our emotional feelings - cutting the sensory nerves between the internal organ and the central nervous system does not abolish emotional behaviour in animals - injecting hormones or artificially activating the autonomic nervous system does not reliably or consistently produce specific emotions
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what does the central nucleus of the amygdala regulate?
emotional response particularly fear responses the central nucleus of the amygdala sends information to various brain structures which control different emotional responses
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what do lesions to the central nucleus to the amygdala do?
reduce/eliminate innate and learned fear responses (all aspects: behavioural, autonomic, and hormonal) but fear of suffocation is normal (or heightened) in people with bilateral amygdala damage
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what does stimulation of the central nucleus of the amygdala cause?
fear, anxiety, and agitation persistent stimulation can promote stress induced illnesses (e.g., ulcers)
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what does viewing threatening stimuli or fearful faces activate in the brain?
the central amygdala which receives inputs from several visual areas (superior colliculi, visual thalamus, and visual association cortex)
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what does damage to primary visual cortex or visual association cortex affect in people in relation to amygdala activity?
patients with damage to primary visual cortex or visual association cortex may have no conscious awareness of looking at a person's face, yet they still show amygdala activity in response to viewing faces and often mimic the presented facial reaction (happy or fearful face)
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what does an bilateral amygdalectomy imply for being able to identify expressions of fear in others?
patient S. P. received a bilateral amygdalectomy to treat a seizure disorder - afterwards she no longer experienced any fear she also could not identify expressions of fear in photos of faces - she had no trouble recognizing specific of faces, but she could not identify when they exhibited fear she could generate artificial expressions of emotion (including fear) without problem, but she could not identify the emotion of fear even in photos of herself - to a lesser extent, but still significant, she also had diminished ability to recognize disgust, sadness, and happiness - her ability to detect surprise and anger were unimpaired
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explain what eye movements and fixations have to do with recognizing emotion
people tend to spontaneously look at and examine the eyes of faces to detect the emotional state of the person they are interacting with S. M. is a patient with bilateral amygdala damage - when shown photographs of faces, she doesn't look at the eyes S. M. can recognize the emotion if she is trained to look at the eyes, but she doesn't do it spontaneously; she has to be reminded every time
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how does recognition of emotion work beyond the amygdala?
beyond the amygdala, many brain areas are activated when we view emotional faces, including the somatosensory cortex, insular cortex, premotor cortex, and cingulate cortex it seems that all these brain regions, particularly in the right cerebral hemisphere, are involved in recognizing emotions in others some people with damage in these regions cannot identify emotional facial expressions in other people
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what are mirror neurons?
mirror neurons are neurons that are activated similarly when an animal performs a particular behaviour or when it sees another animal performing that behaviour mirror neurons have been found in many brain areas: somatosensory cortex, insular cortex, premotor cortex, and cingulate cortex mirror neurons are thought to be involved in mimicry and empathy - it may be that when we see facial expressions, we unconsciously imagine ourselves making that expression, we (internally) imitate what we see the somatosensory cortex may encode representations of what emotions "feel" like (proprioceptively, kinaesthetically) - knowing what it feels like to make a perceived expression, may help us recognize the emotion being expressed in the face we are viewing most human fears are probably acquired socially, not through firsthand experience with painful stimuli, and activation of the mirror neuron system may promote certain types of indirect learning
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how can we recognize emotions in other people by the sound of their voice and choice of words?
word comprehension is generally located in the left cerebral hemisphere for most people however, inferring emotions from the sound (tone) of someone's voice primarily involves the right cerebral hemisphere the amygdala is not strongly involved in either case
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describe prefrontal control of emotions
ROLE OF VENTROMEDIAL PREFRONTAL CORTEX (vmPFC): - involved in regulating expressions of emotions; usually has an inhibitory influence when learned fear responses (e.g., tone --> fear) are extinguished (tone --> now neutral again), this extinction learning involves strengthening of vmPFC connections to the amygdala - lesioning this pathway selectively disrupts extinction learning (but does not disrupt the original fear memory) people with damage to their vmPFC often struggle to control their emotions - in this respect, they act more childlike people with a healthy vmPFC can usually calm themselves when they get frustrated and thus suppress emotional outbursts
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What do the connections between the amygdala and the PFC do for emotional responses in social situations?
the PFC has inhibitory connections with the amygdala which are responsible for suppressing emotional responses in social situations
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explain the case of Phineas Gage
in the mid 1800s, Phineas Gage was a victim of a tragic construction accident an explosion sent a 3cm thick, 90cm long tamping rod through his face, skull and brain before his injury, he was a good natured, kind, responsible, well-liked and respectable man after his injury, he became childish, irresponsible and thoughtless of others - he had severe temper outbursts and used profane language - he was unable to make plans or carry them out - he lost hist job and was unable to keep a social network of friends
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what is the relation between anger, aggression, and impulse control, and the vmPFC?
cognitive abilities are not strongly affected by damage to the vmPFC but vmPFC damage can severely weaken behavioural control and impair decision-making these impairments appear to be a consequence of emotional dysregulation
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What does serotonin levels have to do with risky behaviour and impulse control?
there is a small correlation between risky behaviour, impulsive aggression and low serotonin levels the serotonin metabolite 5-HIAA was measured in the cerebrospinal fluid of rhesus monkeys, which were tracked over 4 years the monkeys with the lowest levels of 5-HIAA were risk takers - they took dangerous unprovoked leaps between trees and were highly aggressive towards older, dominant males - they typically died early from attacks by stronger monkeys in humans, low cerebrospinal 5-HIAA has been associated with aggression and antisocial behaviour, including assault, arson, murder, and child beating drugs that increase serotonin signalling, such as SSRIs like Prozac, tend to decrease irritability and aggressiveness
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what is ingestive behaviour?
eating or drinking
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what is homeostasis?
process by which substances in the body (e.g., sugar) and characteristics of the body (e.g.,s temperature) are maintained at an optimal level
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what is a system variable?
variable that is controlled by a regulatory system for example: temperature in a heating system
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what is a set point?
optimal value of the system variable the goal of a regulatory system is often to keep the system variable near, above, or below some set point
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what is a correlational mechanism?
mechanism of a regulatory process that can control the regulated system variable
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what is a negative feedback?
process by which the effect of a correctional mechanism diminishes or terminates further corrective action a key characteristic of regulatory systems
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what is a satiety mechanism?
brain mechanism that causes cessation of hunger or thirst satiety is associated with 1) adequate supplies of readily available food and water 2) adequate long-term supply of fat satiety can be triggered when food and water are ingested, before most cells in the body have access to them
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how do we monitor water levels?
in two ways our sensation of thirst is related to 1) not enough water inside cells (osmometric thirst) 2) not enough blood/fluid in our circulatory system (volumetric thirst)
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how do our cells get salt?
our cells take in salt from the interstitial fluid as needed water goes wherever salt concentrations are highest (inside or outside of cells) - when we drink water, our cells physically expand in size as they absorb water from the interstitial fluid - when we consume excess salt, our cells physically shrink as they lose water to the salty interstitial fluid - this triggers a type of thirst known as osmometric thirst
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what does tonicity mean?
tonicity refers to the relative concentration of dissolved solutes (e.g., salts) on either side of a membrane that is permeable to water it describes the direction and amount of water flow across the membrane (i.e., osmosis)
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define osmometric thirst
isotonic solution - similar concentrations of solute on either side of the membrane - the cell will neither gain nor lose water hypotonic solution - solute is more concentrated inside the cell than out, so water will enter the cell hypertonic solution - solute is more concentrated outside the cell than in, so water will leave the cell - cause cellular dehydration (water leaves the cell) some neurons in the AV3V region of the hypothalamus are sensitive to angiotensin (volumetric thirst) - other neurons in this area are osmoreceptors (osmometric thirst) - many AV3V neurons exhibit both qualities in human fMRI studies, ingestion of hypertonic saline activates neurons in the AV3V region as well as anterior cingulate cortex drinking water immediately quenches thirst and reduces thirst-related activity in the anterior cingulate, which demonstrates the existence of a rapid feedback mechanism - in contrast, AV3V neurons mostly remain active if their osmoreceptor neurons remain active cold sensors in the mouth and sensory fibers in the stomach are part of the rapid satiety feedback mechanism
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what are osmoreceptors?
neurons that detect changes in cell size the membrane potential and release of neurotransmitter from osmoreceptor cells relates to the volume of these cells
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define volumetric thirst
volumetric thirst occurs when there is not enough blood circulating in the body, which is called hypovolemia - the heart needs a certain amount of blood to keep beating people feel an intense thirst after they lose lots of blood because hypovolemia causes volumetric thirst blood flow (blood volume) is monitored by the kidneys - low blood flow causes the kidneys to release renin, which triggers a hormone signalling cascade that promotes thirst, among other things the feeling of thirst is related to the activation of hypothalamic neurons near the anteroventral tip of the third ventricle (the AV3V region), where the blood brain barrier is weak
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what does food mostly consist of?
sugars (carbohydrates) lipids (triglycerides) amino acids (proteins)
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what does the pancreas do for ingestion?
the pancreas detects blood glucose levels - when blood glucose levels are high, the pancreas releases insulin which causes liver and muscle cells to store glucose as glycogen - when blood glucose levels are low, the pancreas releases glucagon, which causes liver and muscle cells to convert glycogen back into glucose cells internalize glucose with a glucose transporter - cells outside the brain have a glucose transporter that requires insulin to be functional - therefore, cells outside the brain can only use glucose when there is an excess amount of it in the body (signalled by insulin) - when insulin is not around, cells in the body (outside the brain) must break down fatty acids to create glucose for energy - cells within the brain have an additional glucose transporter that works in the absence of insulin, so brain cells can always take in sugar
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what is glycogen?
a polysaccharide, often referred to as animal starch, that constitutes our short-term store of nutrients it is stored in liver and muscle cells
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what is insulin?
pancreatic hormone that facilitates: 1) entry of glucose into cells of the body for immediate use 2) conversion of glucose into glycogen for short-term storage 3) storage of fatty acids as triglycerides in adipose tissue (fat cells) for long-term storage
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What is glucagon?
pancreatic hormone that promotes: 1) conversion of liver glycogen into sugar for immediate use 2) conversion of adipose triglycerides into fatty acids (which will be taken up by cells of the body and converted to sugar for immediate use)
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what is triglyceride?
form of fat storage in adipose cells (fat cells) - constitutes our long-term store of nutrients consists of a molecule of glycerol and three fatty acids
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what is glycerol?
substance derived from breakdown of triglycerides is converted into sugar in the liver when needed
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what is a fatty acid?
substance derived from breakdown of triglycerides is converted into sugar by cells outside the brain when needed
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what does the absence of insulin mean?
that most of cells of boy can no longer use glucose thus, all glucose present in blood is reserved for the central nervous system
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what do the signals from the stomach do for us?
although many factors influence feelings of hunger (sight, sound, smell, taste, time of day, habits, thoughts, etc.), a particularly influential signal comes from the empty stomach an empty stomach (technically an empty duodenum) is communicated to the brain by the stomach's release of a peptide called ghrelin levels of circulating ghrelin increase with hunger and fall with satiation - exogenous administration of ghrelin increases hunger and food intake
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What starts a meal?
ghrelin - peptide hormone released by the empty stomach that increases eating - also produced by neuron in the brain duodenum - first portion of small intestine, attached directly to the stomach - the presence or absence of food in the duodenum regulates the release of ghrelin from the stomach
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What stops a meal?
gastric factors - swelling of the stomach can slightly reduce hunger, but it mostly just causes a bloated feeling - more important are the short-term satiety (fullness) signals released by the stomach and duodenum immediately after eating, before food has been digested - the most prominent among these are CCK and GLP-1, which are regulators of digestive processes - CCK causes the gallbladder to release digestive enzymes into the duodenum - GLP-1 regulates insulin secretion from the pancreas - these peptides are secreted from the duodenum in response to food intake in proportion to the calories ingested - the entry of these molecules into the brain correlates with feelings of satiety and inhibits food intake - repeated administration of CCK to healthy people does not reliably cause sustained weight loss - it may decrease meal size, but people typically respond by eating small meals more frequently - GLP-1 agonists have proven to be more effective for reducing hunger and weight
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what happens after the meal ends?
the satiety produced by gastric and duodenal factors (CCK and GLP-1) is anticipatory (your cells haven't received the nutrients yet) these factors signal that the food in the digestive system, so there should soon be nutrients available to cells elsewhere in the body the last stage of satiety is signalled by the liver and pancreas, as they detect when food has been absorbed into the blood from the intestines the liver measures glucose and free fatty acids levels in the blood - it signals satiety through the 10th cranial nerve (vagus nerve) the pancreas also monitors the blood and releases insulin when blood-glucose levels are elevated - some insulin enters the brain where it acts as a satiety signal - the detection of insulin by neurons in the hypothalamus reduces feelings of hunger
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What do signals from adipose tissue do for long-term satiety?
in most people (and in other animals), body weight seems to be regulated over a long-term basis if a healthy animal is force-fed so that it becomes fatter than normal, it will reduce its food intake once it is permitted to choose how much to eat
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What is leptin?
leptin is a circulating hormone that is secreted by adipocytes (fat cells) - leptin is thought to signal the size of peripheral energy stores in the body as fat cells (energy stores) grow and proliferate, there is a concomitant increase in leptin levels in the blood stream - leptin provides a negative feedback signal that decreases hunger - leptin also increases the sensitivity of hypothalamic neurons to short-term satiety signals exogenous administration of leptin typically decreases meal size in healthy people, but this effect is short-lived artificially increasing leptin levels long-term does not reliably cause weight loss in seemingly any patient population (except for people who are completely unable to produce leptin from birth)
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what is an Ob mouse?
strain of mice whose obesity and low metabolic rate are caused by a mutation that prevents production of leptin
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when are emergency hunger circuits activated?
when a specific critical need to eat or not eat overrides energy homeostasis circuitry
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what is glucoprivation (hypoglycemia)?
dangerously low blood-glucose levels (i.e., not enough immediately available sugar in the blood) - detected by the liver, pancreas, and brainstem can be caused by excess insulin signalling or by drugs that inhibit glucose metabolism
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what is lipoprivation?
dangerously low levels of fatty acids (i.e., not enough fat on the body or not enough free fat acids in the blood) - detected in the hypothalamus (via leptin) and in the liver can be caused by drugs that inhibit fatty acid metabolism
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what happens when someone suffers from hypoglycemia (low blood sugar)?
when the brain senses that it does not have enough glucose (sugar) to support normal brain function (via glucose-sensing neurons in various regions of the brain), it launches an emergency cascade of effects - suppresses insulin secretion to keep sugar in the blood - triggers glucose production in the liver - slows energy expenditure (basal metabolic rate), halting growth and reproductive systems - promotes a potent and sustained feeling of hunger hypoglycemia-induced hunger overrides other homeostatic signals, as it stimulates hunger irrespective of the amount of other short- and long-term satiety molecules - excess insulin can trigger hypoglycemia and intense hunger because it causes glucose to be stored in muscle and fat cells for later use
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what happens when someone suffers from lipoprivation (not enough body fat)?
when the brain detects dangerously low leptin levels, it thinks the body does not have enough fat on it to support long-term energy homeostasis - this launches an emergency cascade of effects that are almost identical to those observed in response to low blood sugar dangerously low levels of body fat (signalled by insufficient leptin) trigger the same emergency feeding circuits as dangerously low levels of glucose - it is an orchestrated response to raise blood-glucose levels diabetes: disruptions in insulin signalling cause high blood sugar (hyperglycemia), since the sugar in the blood will not get converted into glycogen or fat for long-term storage - if left untreated, this causes progressive weight loss - the resulting drop in body fat and leptin signalling can initiate intense hunger, even if the person is hyperglycemic (too much blood sugar) - this used to happen to diabetics and often led to death before insulin treatments were discovered 100 years ago
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how does leptin regulate hunger and basal metabolic rate?
by acting on leptin receptors throughout the brain
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what strongly influences the feelings of hunger?
two groups of neurons in the arcuate nucleus of the hypothalamus - leptin regialtes the activity of these cell population in an opposing manner in the arcuate nucleus of the hypothalamus: - leptin inhibits AGRP/NPY neurons - leptin activates POMC/α-MSH neurons leptin also makes these neurons more sensitive to satiety peptides such as CCK and less sensitive to hunger peptides such as ghrelin
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what does the arcuate nucleus (ARC) of the hypothalamus do for hunger?
AGRP/NPY neurons promote hunger - these neurons are inhibited by leptin and activated by ghrelin POMC/α-MSH neurons inhibit hunger - these cells are activated by leptin and inhibited by ghrelin the activity of these cells can have an immediate effect on hunger - for example, stimulation of AGRP/NPY neurons causes voracious eating to some extent, the balance of activity between these two cell populations may determine how much fat the brain thinks it is necessary to have on the body
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what is the arcuate nucleus of the hypothalamus?
nucleus in base of hypothalamus that ocntains neurons hgihly sensitive to circulating levels of leptin contains AGRP/NPY neurons and POMC/α-MSH neurons, which are involved in controlling hunger and basal metabolic rate
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what is the paraventricular nucleus (PVN) of the hypothalamus?
nucleus of hypothalamus that receives inputs from neurons in the arcuate nucleus contains a collection of neurons that stop firing when the body has dangerously low levels of fat (leptin) when leptin levels fall to critically low levels (indicating there is not enough body fat), some neurons in the paraventricular nucleus (PVN) of the hypothalamus stop firing when these neurons stop firing, animals feel intense hunger artificially increasing PVN neuron activity does not block other homeostatic controllers of hunger, so this region is thought to play a special role in low leptin-induced emergency feeding
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What is Prader-Willi syndrome?
prader-willi syndrome is a rare chromosomal abnormality in which up to 7 genes are deleted from chromosome 15 - one of these genes is critical for the development/survival of certain neurons in the PVN people with prader-willi syndrome are born with very low muscle mass and have little interst in eating - but later, between 2 and 8 years old, these people develop a heightened, permanent and painful sensation of hunger, a feeking of starving to death - average life expectancy in the US is 30; most die of obesity-related causes people with this disorder have no sensations of satiety to tell them to stop eating or to throw up, so they can accidentally consume enough food in a single binge to fatally rupture their stomach
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moderan obesity epidemic and leptin
about 50% of the variability in people's body fat is due to genetic differences natural variations in metabolic efficiency are one of the most important factors - however, the hunger system of overweight individuals seems to actively defend its elevated levels of body fat - they seem to have an elevated leptin set point that they are trying to maintain, and they have a blunted response to increases in leptin levels this is called leptin resistance - in different population of overweight animals, researchers have observed - a reduction in leptin's ability to cross the blood-brain barrier - a reduction in hypothalamic neurons' responses to leptin signalling after several days of eating a cafeteria-style diet (high fat, high sugar), inflammation has been observed in the hypothalamic arcuate nucleus of rodents - this may somehow cause these neurons to become less sensitive to leptin signalling leptin-resistant animals seem to require more leptin in their blood (more fat cells on their body) to achieve their body fat homeostatic set point - yet, we know it is more complicated than this, since repeated injections of leptin does not reduce body weight
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What are hedonic aspects of hunger?
the hedonic aspects of hunger refer to the motivational and reinforcing properties of food, which fluctuate in accordance with hunger - hunger increases the rewarding and reinforcing value of food - satiety reduces the rewarding and reinforcing value of food but when you are hungry, how much of a priority is it to you? - it is all you can think about, or is it just something to keep in the back of your mind? - does food taste amazing or is it just satisfying? neurons in the medulla and hypothalamus orchestrate these motivational and hedonic effects by releasing specific neuropeptides throughout the brain - the neuropeptides GLP-1, NPY, orexin, and MCH all play an important role in regulating these aspects of hunger all these signalling molecules (with leptin and ghrelin) influence dopamine neuron activity, which regulates motivation and reinforcement learning
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explain surgical treatments for obesity
surgeries have developed that are designed to reduce the amount of food that can be eaten during a meal or interfere with absorption of calories from the intestines bariatric surgery modifies the stomach, small intestines, or both - the most effective form of bariatric surgery is called the Roux-en-Y gastric bypass (RYGB) with RYGB surgery, the jejunum (second part of small intestine, immediately downstream from the duodenum) is cut and the bottom part is attached to the stomach rats that have the RYGB procedure eat less and lose weight reductions in hunger are often observed in people over time, but it is not clear why this happens the surgery does alter the release of gastric hunger and satiety signals, but other (unknown) factors are thought to play a more important role
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what is learning?
learnign refers to the process by which experiences change our nervous system and hence our behaviour we refer to these changes as memories (memory traces or memory engrams) - memory can be transient or durable, explicit or implicit, personal or impersonal accessing memories is known as memory retrieval
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What is neuronal plasticity?
the cellular basis of long-term memory is neuronal plasticity, which refers to the ability of the nervous system to change and adapt
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what did researchers measure to identify neuronal plasticity?
intrinsic excitability - the number of action potentials a neuron exhibits in response to an influx of positive current synaptic strength - the amount of positive (or negative) current that enters the postsynaptic neuron when a presynaptic cell has an action potential - a change in the strength of the synaptic connection between two neurons is called synaptic plasticity
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how is intrinsic excitability determined?
by the number and type of ion channels (leak channels and voltage-gated channels) expressed by the neuron if a neuron starts making fewer potassium leak channels, its resting membrane potential will be slightly depolarized, which means the neuron will be more excitable in general (i.e., it will exhibit more action potentials in response to the same excitatory synaptic input)
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what is synaptic plasticity?
it refers to changes in the strength of the synaptic connection between two neurons when a presynaptic cell releases neurotransmitters, how big or how small is the postsynaptic response (regardless of whether it is depolarization or hyperpolarization)? if the postsynaptic response is depolarization, we call it an EPSP synaptic plasticity can involve pre- and postsynaptic changes - on the presynaptic side, the amount of voltage-gated calcium channels on the presynaptic membrane influences how many vesicles will be released following an action potential - on the postsynaptic side, the amount of neurotransmitter receptors influence the sensitivity of the postsynaptic cell to neurotransmitter release
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describe habituation and sensitization in the aplysia (sea slug)
it has a large gill for respiration, and a siphon through which it expels water if the siphon is lightly touched, the gill withdraws reflexively repeated light touching of the siphon will reduce the magnitude of this reflex until the Aplysia completely ignores light touches this is an example of habituation - reduced physiological or behavioural responding to a repeated stimulus in contrast, in response to painful electrical shocks, the sea slug's gill withdrawal reflex becomes stronger - increased sensitivity to a stimulus is known as sensitization
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how can cell excitability and synaptic strength be directly measured?
in brain slice recordings
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what is long-term potentiation (LTP)
long-term increase in the strength of the connection between two neurons (i.e., increased synaptic strength) repeated high-frequency (tetanic) stimulation of the inputs to a neuron often induces LTP - commonly used is 100 Hz stimulation for 1 second (repeated 4 times) LTP is often initiated on the postsynaptic side (with more neurotransmitter receptors) but retrograde signalling of nitric oxide (NO) can drive presynaptic modifications (e.g., more vesicles of neurotransmitters)
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what is long-term depression (LTD)?
long-term decrease in the strength of the connection between two neurons (i.e., decreased synaptic strength) persistent low-frequency stimulation of the inputs to a quiet neuron often causes LTD - commonly used is 1 Hz stimulation for 10 minutes LTD is often initiated on the postsynaptic side (with less neurotransmitter receptors) but retrograde endocannabinoid signalling can drive presynaptic modifications (e.g., less calcium-influx per action potential)
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why does the same number of stimulations delivered at different rates cause opposing effects; LTP and LTD?
it turns out that LTP and LTD are a function of the number of times the synapse was activated as well as whether the postsynaptic neuron fired at those precise times for LTP to occur, the release of neurotransmitter must coincide with a substantial depolarization of the postsynaptic cell (normally associated with an action potential) high frequency axon stimulation often causes postsynaptic neurons to spike (summation of EPSPs brings the neuron across threshold) - low frequency stimulation on its own is often not sufficient to get a postsynaptic neuron to spike
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what is an NMDA receptor?
NMDA glutamate receptor - a coincidence detector NMDA receptors play a large role in learning and memory - they are located in almost every glutamatergic synapse in the brain the NMDA receptor is an ionotropic glutamate receptor that has a large ion pore - when the NMDA receptor binds glutamate and opens, magnesium ions (Mg2+) try to pass through its pore, but they get stuck in it and block all current flow - the Mg2+ blockage of the threshold (< -40 mV), such as when the cell is at rest if the membrane is depolarized (i..e, more positive than -40 mV) because of other synaptic inputs, then Mg2+ ions will not try to enter through the NMDA receptor, and thus they won't clog the pore so, current flow through the NMDA channel is gated by both glutamate and membrane voltage - Na+ and Ca2+ ions will enter a cell through NMDA receptors, but only when these receptors are bound to glutamate and Mg2+ is not clogging the pore
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what is an AMPA receptor?
the glutamate receptor that mediates most excitatory fast synaptic currents in the brain - it is ionotropic and opens upon glutamate binding it lets in sodium ions which causes EPSPs that depolarizes neurons most glutamate synapses in the brain have AMPA and NMDA receptors
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What is an NMDA receptor?
ionotropic glutamate receptor that only passes current upon glutamate binding when the membrane potential is slightly depolarized if glutamate binds when the cell is hyperpolarized, the pore will get blocked by Mg2+ open, unblocked NMDA receptors allow sodium and calcium ions through
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what is CaMKII?
type II calcium-calmodulin kinase it is an enzyme that is activated by calcium influx through NMDA receptors - it plays a role in the intracellular signalling cascade that establishes long-term potentiation, by increasing the number of postsynaptic AMPA receptors (in excitatory glutamatergic synapses)
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what does the strength of glutamate synapses strongly correlate with?
the size of the postsynaptic dendritic spine and the number of AMPA glutamate receptors in it
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How else can LTP be expressed?
LTP can also be expressed through changes on the presynaptic side of things, but postsynaptic neurons often initiate the process - many experiments suggest that nitric oxide (NO) can act as a retrograde messenger (released from postsynaptic membrane and detected by presynaptic membrane) to promote LTP
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what is associative long-term potentiation?
the increase in synaptic strength that occurs in weak synapses when they are active right around the time when stronger inputs caused the postsynaptic neuron to spike
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What is Hebb's rule?
hypothesis proposed by Donald Hebb that the cellular basis of learning involves the strengthening of synaptic connections that are active when the postsynaptic neuron fires an action potential this is known as: fire together, wire together... more strongly than before - the synaptic connection does have to initially exist
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What is perceptual learning?
learning to recognize stimuli as distinct entities
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what is motor learning?
learning to make skilled, choreographed movements procedural learning
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what is relational learning?
learning relationships among individual stimuli stimulus-stimulus learning
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what is stimulus-response learning?
learning to perform a particular behaviour when a particular stimulus is present includes classical and instrumental conditioning