Midterm 2 Flashcards

1
Q

What is sensation?

A

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

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2
Q

What is perception?

A

Refers to the conscious experience and interpretation of sensory information

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3
Q

What happens first: perception or sensation?

A

Sensation is the initial process and perception is making something of the sensation

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4
Q

What are sensory neurons/sensory receptors?

A
  • Specialized neurons that detect a specific category of physical events.
  • They accomplish this task with receptor proteins that they put on the membrane which are sensitive to specific sensory stimuli/specific features of the extracellular environment
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5
Q

List the specific sensory stimuli/specific features of the extracellular environment that receptor proteins are sensitive to?

A
  • the presence of specific molecules (via chemical interactions)
  • physical pressure
  • temperature
  • pH (acidity, basicity)
  • electromagnetic radiation (light)
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6
Q

What kind of extra sensory stimuli/specific features of the extracellular environment are non-human animals’ receptor proteins sensitive to?

A
  • Electrical and magnetic fields
  • Humidity
  • Water pressure
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7
Q

What happens if it gets too hot or too cold?

A

Ion channels open if it gets too hot or too cold and this triggers an action potential

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8
Q

What’s sensory transduction?

A

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

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9
Q

What’s a receptor potential?

A
  • Graded change in the membrane potential of a sensory neuron caused by sensory stimuli
  • Sensory stimuli being detected by sensory neurons
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10
Q

What’s a sensory neuron?

A

Specialized neuron that detects a particular category of physical events (sensory stimuli)
Ex: photoreceptor cells transduce light into receptor potentials

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11
Q

What do all sensory neurons do and what do they don’t all do/have?

A
  • All sensory neurons release neurotransmitters
  • Not all sensory neurons have axons or action potentials
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12
Q

How do smaller cell sensory neurons, such as photoreceptor neurons, who don’t have action potentials release neurotransmitters?

A
  • They release neurotransmitter in a graded fashion, dependent on their membrane potential
  • The more depolarized they are, the more neurotransmitter (ex: glutamate for photoreceptors) they release
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13
Q

What’s an example of a cell that is a sensory neuron who does not have an axon or action potentials?

A

Photoreceptor cells

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14
Q

What are opsins and what kind of metabotropic receptors are they?

A
  • Receptor proteins that are sensitive to light -> they detect light
  • Many opsins gain their sensitivity to light by binding to a molecule of retinal
  • The opsins in our eye that transduce visual information are all inhibitory metabotropic receptors
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15
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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16
Q

What are the four different types of photoreceptor cells we have and what do they express?

A
  • Rod cells (express rhodopsin)
  • Red cone cells (express red cone opsin)
  • Green cone cells (express green cone opsin)
  • Blue cone cells (express blue cone opsin)
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17
Q

How many of the different types of opsins does each photoreceptor cell in our eye contain?

A

Each photoreceptor cell in our eye contains only one of these types of opsins

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18
Q

What’s a photoreceptor cell?

A
  • Sensory neuron responsible for vision
  • These cells transduce electromagnetic energy from visible light into receptor potentials
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19
Q

What’s the retinal and what kind of wavelength of light does it interact with?

A
  • Small molecule (synthesized from vitamin A) that binds to opsin proteins and changes its physical shape when it absorbs light
  • In mammals, retinal is the actual molecule that absorbs the energy of photons
  • The wavelength of light that retinal can interact with is dependent on the opsin protein that retinal is bound to
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20
Q

Where is the opsin protein located?

A

It is embedded in the membrane of photoreceptor cells

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21
Q

What happens when light hits one electron in the retinal molecule?

A

That electron absorbs the light and goes into a high-energy state

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22
Q

What does visible light refer to and how do we detect this light?

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 & 3 cone cells)
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23
Q

What kind of light are rod cells very sensitive to?

A

They’re very sensitive to all visible light

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24
Q

True or False? All light travels at different speeds

A

False, all light travels at the same speed

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25
Q

What does the wavelength of the light signify?

A

How much energy the light has

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26
Q

How do cone cells interact with light?

A
  • They’re not particularly sensitive to light
  • There are 3 different kinds of them, each sensitive to different wavelengths
  • They encode color vision
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27
Q

As you move from Gamma rays to TV and Radio Waves, how does the wavelength and energy vary?

A

Gamma rays have small wavelengths but high energy and these get progressively bigger and stronger till’ Tv and Radio waves which have long wavelengths and lower energy

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28
Q

Which opsin in our eyes first evolved hundreds of million years ago?

A

The red cone cell (red cone opsin)

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29
Q

How does the detection of light vary with how many cone cells you have in your eyes?

A
  • 1 cone (red cone) = I see light or I don’t see light
  • Once you have 2 cones you have colour
  • Once you have 3 cones, you can differentiate the entire colour spectrum
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30
Q

What kind of light activates the blue cone opsin?

A

Purple light

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31
Q

What kind of light activates the red cone opsin?

A

Pure red light

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32
Q

Is there colour in the peripheral vision?

A

The peripheral vision isn’t used to detect colour but is only used to detect stimuli

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33
Q

What kind of wavelengths of light are blue cone opsins most sensitive to?

A

Blue cone opsins are most sensitive to short wavelengths

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34
Q

What kind of wavelengths of light are green cone opsins most sensitive to?

A

Green cone opsins are most sensitive to medium wavelengths

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35
Q

What kind of wavelengths of light are red cone opsins most sensitive to?

A

Red cone opsins are most sensitive to long wavelengths

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36
Q

What is colour perception a function of?

A

A function of the relative rates (ratio) of activity in the 3 types of cone cells

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37
Q

What determines the amount of activation of any cone?

A

Both on the wavelength of the light and the amount of it (its intensity)

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38
Q

Which of the 3 cone opsins is most sensitive to light?

A
  • Green cone opsins are the most sensitive to light, so if shown 3 colors separately (blue, green & red) at the same intensity, people often say the green light is brighter
  • Blue cones are the least sensitive to light
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39
Q

What happens when red and green light bulbs are too close together?

A

Our eyes have a harder time differentiating them, they end up just looking yellow to us

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40
Q

How is paint different from light?

A
  • Paint doesn’t create light; it absorbs some and reflects some
  • Paint is considered subtractive of light whereas light is considered additive of light
  • 3 primary colours for paint: yellow magenta and cyan
  • 3 primary colours for light: green, red and blue
  • The colours of paint only subtract one coloured light at a time
  • When mixed together, paint is black (absence of colour)
  • When mixed together, light is white (all the colours all at once and all light bouncing off of white)
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41
Q

What are the 3 dimensions to our perception of light and color?

A
  • Brightness (intensity)
  • Saturation (purity of wavelength)
  • Hue (dominant wavelength - colour)
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42
Q

What happens if brightness is 0%?

A

The image will be black and hue and saturation will have no impact

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43
Q

What happens if saturation is 0%?

A

You’ll find yourself in the middle of the color cone where there is no color (equal contribution from all wavelengths) which results in a black and white image

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44
Q

What is Protanopia?

A
  • Colour vision deficiency
  • Absence of the red cone opsin (1% of males)
  • Visual acuity is normal because red cone cells get filled with green cone opsin
  • Inherited
  • People have trouble distinguishing colors in the green-yellow-red section of the spectrum
  • Simple mutations of the red cone opsin (1% of males) produce less pronounced deficits in color vision
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45
Q

What is Deuteranopia?

A
  • Colour vision deficiency
  • Absence of the green cone opsin (1% of males) - Visual acuity is normal because green cone cells get filled with red cone opsin
  • Inherited
  • People have trouble distinguishing colors in the green-yellow-red section of the spectrum
  • Simple mutations in of the green cone opsin (6% of males) produce less pronounced deficits in color vision
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46
Q

What’s Tritanopia?

A
  • Colour vision deficiency
  • Absence of the blue cone opsin (1% of the population)
  • Blue cone cells don’t compensate for this in any way, but blue cone opsin is not that sensitive to light, so visual acuity is not noticeably affected
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47
Q

Why is colour blindness way more prominent among men?

A

Since they only have one X chromosome

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48
Q

What’s achromatopsia?

A
  • True color blindness
  • Typically caused by mutations in the g protein signaling cascade that is similar in all cone cells
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49
Q

What’s the cornea?

A
  • The outer, front layer of the eye
  • Focuses incoming light a fixed amount
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50
Q

What’s the iris?

A

A pigmented ring of muscles

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51
Q

What’s the conjunctiva?

A
  • Mucous membranes that line the eyelid
  • They’re fused with our eyes -> why you can’t get things behind your eye
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52
Q

What’s the lens?

A
  • Consists of several transparent layers
  • The shape of the lens can change to allow the eye to focus, a process known as accommodation
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53
Q

What’s the pupil?

A
  • Regulates the
    amount of light entering the eye
  • It’s an opening in the iris
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54
Q

How could mutations of the cornea affect your vision?

A

Cornea being too thick or thin will affect your vision

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55
Q

What’s the retina?

A
  • The interior lining (furthest back part) of the eye
  • Contains photoreceptor cells
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56
Q

What’s the fovea?

A
  • The central region of the retina
  • There’s very little compression of visual information in the fovea, so this is where we have the highest visual acuity
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57
Q

What’s the optic disk?

A
  • Site of blind spot in eye
  • The point at which the optic nerve exits through the back of the eye
  • It has no receptors
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58
Q

How can photoreceptors in the fovea register the exact location of the input, which enables high resolution, color vision?

A

Because the fovea primarily contains cone cells, each of which connects to a single downstream collection of cells (a bipolar cell which in turn connect to a single ganglion cell)

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59
Q

What is foveal vision sensitive to?

A

Detail & color

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60
Q

What is peripheral vision sensitive to?

A

Dim light

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61
Q

Why is precise location and shape of input heavily impeded in the periphery?

A

Because collections of photoreceptors (primarily rods, which use the opsin rhodopsin) converge onto fewer and fewer downstream collections of neurons (bipolar and ganglion cells)

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62
Q

How many more bipolar cells does the periphery have compared to the fovea?

A

10 x the amount of bipolar cells

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63
Q

How large is our field of vision and how much of it can we accurately read?

A
  • Our field of vision is 120º
  • We can only read in 2º of our vision (with our fovea) everything else is too blurry to make out
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64
Q

Describe the primary characteristics of cones

A
  • Most prevalent in the central retina; found in the fovea
  • Sensitive to moderate-to-high levels of light
  • Provide information about hue
  • Provide excellent acuity
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65
Q

Describe the primary characteristics of rods

A
  • Most prevalent in the peripheral retina; not found in the fovea
  • Sensitive to low levels of light
  • Provide only monochromatic information
  • Provide poor acuity
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66
Q

What are orbits?

A

Bony sockets in the front of the skull where eyes are suspended

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67
Q

What holds the eye in place and allows it to move around?

A

Six extraocular muscles attached to the sclera

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68
Q

What are saccadic eye movements?

A
  • Rapid, jerky shifts in gaze from one point to another
  • Our eyes scan a scene by making saccadic movements
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69
Q

What are pursuit eye movements?

A
  • Calmer eye movement
  • They allow us to maintain an image of a moving object
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70
Q

What are the 3 neurons in the retina?

A
  • Photoreceptor cells
  • Bipolar cells
  • Ganglion cells
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71
Q

What’s the function of photoreceptor cells as neurons in the retina?

A

Neurons responsible for the transduction of light; they project to bipolar cells

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72
Q

What’s the function of bipolar cells as neurons in the retina?

A

Neurons that relay information from photoreceptor cells to ganglion cells

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73
Q

What’s the function of ganglion cells as neurons in the retina?

A
  • 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 disc
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74
Q

What’s the function of horizontal cells in the retina?

A
  • Neurons that interconnect and regulate the excitability of adjacent photoreceptor and bipolar cells
  • They adjust the sensitivity of these neurons to light in general (adjust the excitability)
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75
Q

What’s the function of amacrine cells in the retina?

A
  • Neurons that interconnect and regulate the excitability of adjacent bipolar and ganglion cells - Many different types of amacrine cells, and each have different functions
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76
Q

What’s the order of the layers of the retina that light passes through?

A
  1. Ganglion cell layer
  2. Bipolar cell layer
  3. Photoreceptor cell layer
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77
Q

What kind of ion channels do photoreceptor cells have in addition to the regular leak potassium ion channels that all neurons have and how do these work?

A
  • “leaky” sodium ion channels which are open in the dark (when the cells are at rest)
  • 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
  • These channels close when the retinal portion of the retinal-opsin complex absorbs light, which hyperpolarizes the membrane to -70 mV
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78
Q

Do bipolar cells have action potentials?

A

Bipolar cells don’t have action potentials and release glutamate in a graded fashion dependent on their membrane potential

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79
Q

What are the 2 types of bipolar cells and describe how these function?

A
  • OFF bipolar cells which express ionotropic glutamate receptors, so they are depolarized by glutamate. Because photoreceptor cells constantly release glutamate in the dark, OFF bipolar cells are more active (more depolarized) in the dark than in the light (release neurotransmitter in dark)
  • 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 (release neurotransmitter in light)
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80
Q

Do retinal ganglion cells have action potentials?

A
  • Yes, they’re typical neurons
  • They have action potentials and are generally excited by glutamate
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81
Q

What’s the receptive field of a neuron involved in visual processing and how is it identified in animals?

A
  • The area of visual space where the presence of light influences the firing rate (or activity) of that neuron
  • As the animal maintains focus on a central fixation point, you shine light in different areas of visual space and see where in visual space a change in light alters the spiking activity of the neuron
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82
Q

Describe how retinal ganglion cells react to light in different ways in their receptive field

A
  • 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 ganglion cells are excited by light in the center and are inhibited by light in the surround
  • OFF cells are excited by light in the surround and are inhibited by light in the center
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83
Q

How does visual information get relayed to the brain?

A

Visual information is relayed from retinal ganglion cells (RGCs) to the thalamus (the lateral geniculate nucleus) to area V1 in the cerebral cortex (primary visual cortex) which is found in the occipital lobe, which then travels through the visual association cortex and goes to the temporal lobe and the parietal lobe

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84
Q

Describe simple cells

A

Simple cells in primary visual cortex are sensitive to lines of light, and their receptive fields are typically organized in a center-surround fashion.

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85
Q

How much of the cerebral cortex is dedicated to processing visual information?

A

20-25%

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86
Q

Describe the visual association cortex?

A
  • Part of the occipital lobe that surrounds primary visual cortex
  • Each area of the visual association cortex responds to particular features of the visual environment, such as particular shapes, locations, movements, and colors
  • Each region forms one or more independent maps of the visual field
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87
Q

Describe the receptive field of neurons in the Primary Visual Cortex

A
  • 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
  • This is because they are trying to identify areas where there are sharp transitions between light and dark (or between two colors) and are hence trying to identify borders, edges, corners
  • Trying to identify objects and their relative position in space
  • This activity done through Top-Down processing
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88
Q

What kind of visual processing does the temporal lobe (ventral stream) do?

A
  • Involved in identifying form (shape)
  • It encodes “what” the object is and its color
  • Most of the information is coming from the fovea, most of it coming from cone cells, that are detecting what colours
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89
Q

What kind of visual processing does the parietal lobe (dorsal stream) do?

A
  • Involved in identifying spatial location
  • It encodes “where” objects are, if they are moving, and how you should move to interact with or avoid them
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90
Q

What’s monocular vision?

A

Some primary visual cortex neurons respond to visual input from just one eye

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91
Q

What’s binocular vision?

A

Most primary visual cortex neurons respond to visual input from both eyes

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92
Q

What’s depth perception?

A
  • Many monocular cues 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
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93
Q

What’s stereopsis?

A

Perception of depth that emerges from the fusion of 2 slightly different projections of an image on the 2 retinas

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94
Q

What’s retinal disparity?

A
  • The difference between the images from the two eyes, which results from their horizontal separation - It improves the precision of depth perception, which is particularly helpful when trying to plan movements to interact with objects in space
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95
Q

What is Agnosia?

A
  • Deficit in the ability to recognize or comprehend certain sensory information, like specific features of objects, persons, sounds, shapes, or smells, although the specific sense is not defective nor is there any significant memory loss
  • Relates to a problem/damage in some sensory association cortex…not to problems with the sensory neurons themselves or with primary sensory areas
  • Problems with comprehending the stimuli and not detecting it
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96
Q

What’s Akinetopsia?

A
  • Deficit in the ability to perceive movement
  • Type of visual agnosia caused by damage in an area of the dorsal visual stream (in the parietal lobe of the cerebral cortex)
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97
Q

What’s Cerebral Achromatopsia?

A
  • Visual agnosia caused by damage to the ventral visual stream (temporal lobe) -> not genetic mutation
  • People will deny having any perception of color and say everything looks dull or drab, and that it is all just “shades of grey”
  • Lose the ability to remember the colour of things from before
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98
Q

What’s Prosopagnosia?

A
  • Failure to recognize particular people by sight of their faces; caused by damage to the fusiform gyrus (fusiform face area)
  • Can detect other people from the smell or sound of them so they don’t notice anything’s wrong
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99
Q

Why are most of the visual pathways bidirectional?

A
  • Their axons go both ways
  • Top-down processing
  • 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)
  • Descending information cancels out the correctly predicted ascending information, so the only information that actually ascends are errors in visual predictions
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100
Q

What’s the predictive coding theory of perception?

A
  • Each level of the visual 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
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101
Q

Which axons leave the eye?

A

Only the axons of retinal ganglion cells

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102
Q

What’s the function of the superior colliculi?

A

Visual information is used here to control fast visually-guided movements (visual reflexes)

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103
Q

What’s the function of the hypothalamus with visual information?

A

Visual information is used here to control circadian rhythms (such as sleep-wake cycles)

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104
Q

What’s the function of the somatosensory system?

A

It provides information about touch, pressure, temperature, and pain, both on the surface of the skin and inside the body

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105
Q

What are the 3 interacting somatosensory systems?

A
  • the exteroceptive system (cutaneous/skin senses)
  • the interoceptive system (organic senses)
  • the proprioceptive (kinesthesia) system
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106
Q

What’s the function of the exteroceptive system?

A

It responds to external stimuli applied to the skin (e.g. touch)

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107
Q

What’s the function of the interoceptive system?

A

It provides information about conditions within the body and is responsible for efficient regulation of its internal milieu (e.g. heart rate, breathing, hunger, bladder)

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108
Q

What’s the function of the proprioreceptive system?

A

It monitors information about the position of the body, posture and movement (e.g., the tension of the muscles inside the body)

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109
Q

What are the different types of external stimuli that cutaneous senses (skin) encode?

A
  • Pressure (touch)
  • Vibrations
  • Temperature
  • Pain
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110
Q

What is skin pressure caused by?

A

Mechanical deformation of the skin

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111
Q

When do skin vibrations occur?

A

When we move our fingers across a rough surface

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112
Q

What is skin temperature caused by?

A

Produced by objects that heat or cool the skin

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113
Q

What is pain on the skin caused by?

A

Can be caused by many different types of stimuli, but primarily tissue damage

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114
Q

What are the different layers of the skin called?

A
  • The outermost layer of skin -> Epidermis, where its cells get oxygen from the air, not the blood
  • The middle layer is called dermis
  • The deepest layer is called the hypodermis (or subcutaneous, “below the skin”)
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115
Q

What’s glabrous skin?

A
  • “Hairless” skin (palm of hands and feet) which are very sensitive parts of our skin and have particular kinds of sensory neurons
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116
Q

What do free nerve endings primarily respond to?

A
  • Temperature and Pain
  • May confuse the two when there are sharp temperature changes (ex: sticking cold hand in warm water will feel like it’s burning sensation)
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117
Q

What are the different corpuscles in the skin and what do they respond/ are sensitive to?

A
  • Ruffini corpuscules -> sensitive to stretch and the kinesthetic sense of finger position and movement
  • Pacinian corpuscles -> respond to skin vibrations
  • Meissner’s corpuscles (only in glabrous skin) -> detect very light touch and localized edge contours (brail-like stimuli)
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118
Q

What are the two categories of thermal receptors?

A

Those that respond to warmth and those that respond to coolness

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119
Q

Describe thermal receptors

A
  • 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 ex: capsaicin molecules activate heat receptors and menthol molecules activate cold receptors
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120
Q

Describe pain receptors

A
  • Mediated by free nerve endings in the skin
  • Many types of pain receptor cells (usually referred to as nociceptors, or “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 something striking, stretching, or pinching the skin
  • Other types of free nerve ending appear to respond to extreme heat (or the presence of chemicals such as capsaicin, the active ingredient in chili peppers)
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121
Q

What is Phantom Limb?

A
  • 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 (cold, itchy, hot, hurts)
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122
Q

What causes phantom limb and what’s the treatment?

A
  • One idea: 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
  • Treatment: behavioural therapy where they put a mirror and gives the brain an opportunity to reconceptualize
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123
Q

How do axons from skin, muscles and internal organs enter the CNS and what are 2 main pathways

A
  • Enter the CNS via spinal nerves
  • 1st pathway: Poorly localized information (crude touch, temperature, and pain) immediately crosses over in the spinal cord and the first synapse is there. This information then ascends to the thalamus through the spinothalamic tract.
  • 2nd pathway: highly localized information (ex: 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 then get bundled together in the midbrain before synapsing in the thalamus. From there, information goes to primary somatosensory cortex in the parietal lobe
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124
Q

What is the somatotopic map of the body surface?

A
  • Map that highlights the relationship between cortical stimulations and body sensations
  • Also referred to as somatosensory homunculus (“little man”)
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125
Q

What’s tactile agnosia?

A
  • Occurs from damage to somatosensory association cortex
  • Patients with tactile agnosia have trouble identifying objects by touch alone and may confuse the object with another one
  • However, these patients can often draw objects that they are touching, without looking, and they can sometimes identify objects from their drawings
  • They can identify the objects by sight
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126
Q

What happens when a tasted molecule binds to a taste receptor protein?

A
  • Produces a change in membrane potential (either directly or through g protein signaling cascades)
  • Different tastes relate to the activation of different types of taste receptor proteins
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127
Q

Describe taste buds

A
  • Taste buds consist of groups of 20 to 50 taste receptor cells
  • Each taste bud is sensitive to a particular type of taste because all the cells in a taste bud express 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 10 days (dying all the time) due to being exposed to hostile environment
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128
Q

What are the 6 different categories of taste receptors and how are they detected ?

A
  • sweetness (sugar) -> detected with a single metabotropic receptor
  • umami (glutamate - found in high protein foods) -> detected with a single metabotropic receptor
  • bitterness (a variety of different molecules) -> detected with 50 different metabotropic receptors
  • saltiness (ions) -> detected with an ion channel that is highly permeable to sodium
  • sourness (pH level; also detects carbonation) ->
    detected with an ion channel that is highly permeable to hydrogen channels
  • fat (fatty acids) -> detected with metabotropic receptors and fatty acid transporters
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129
Q

Which taste receptor cells are instinctively rewarding/reinforcing?

A
  • Sugar and umami taste receptor cells
  • Direct stimulation of them (or their downstream structures in the cerebral cortex) is inherently reinforcing
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130
Q

Which taste receptor has a different type of receptor for every one of its tasting molecules?

A
  • Bitterness
  • Bitter taste is unique
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131
Q

Which taste receptor cells are instinctively aversive?

A
  • Bitter taste receptor cells
  • People often grow to appreciate some bitter taste cell activity at low concentrations (as an acquired taste)
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132
Q

What activates both salt and umami receptors?

A

MSG (monosodium glutamate)

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133
Q

Where is the primary gustatory cortex located?

A

In the insula lobe of the cerebral cortex

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134
Q

What happens to mice when we switch their sugar receptor genes with bitter receptor genes?

A

They can’t taste sugar anymore and begin to enjoy the bitterness

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135
Q

What are the molecules that the olfactory system is specialized for identifying?

A
  • Odorants
  • They are volatile substances
  • Most of them are lipid soluble fats and of organic origin, however many substances that meet these criteria have no odor
  • The receptor proteins that transduce odorants into a change in membrane potential are metabotropic g protein-coupled receptors
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136
Q

Why are dogs much better at smelling than humans?

A
  • Because most odorants are resting on the ground and to detect them you have to sniff and this gust of wind will get them to go up and bind to receptors
  • Dogs are smell-oriented and are always sniffing the ground and are closer to the ground
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137
Q

What’s Olfactory epithelium?

A
  • The tissue of the nasal sinus that sits underneath the skull (the cribriform plate) and contains olfactory receptors cells
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138
Q

How do olfactory cells function?

A
  • Each olfactory cell expresses only one type of olfactory receptor protein
  • Olfactory receptor cells synapse in glomeruli in the olfactory bulb, which in turn sends axons into the brain
  • Each glomerulus processes information from just one type of olfactory receptor cell (expressing a particular type of olfactory receptor protein)
  • Each glomerulus processes a distinct odor
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139
Q

Are odors hardwired to be good or bad to humans?

A

Odors are largely not hard wired to be innately good or bad. Whether we like or dislike an odor is related to learned associations

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140
Q

How is olfactory information relayed to the brain?

A

It goes directly to primary olfactory cortex in the temporal lobe and the amygdala

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141
Q

What are pheromones?

A
  • 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)
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142
Q

What are functions of pheromones in many animals, especially insects?

A
  • 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
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143
Q

Describe what sound waves are

A
  • When an object vibrates, its movement causes the molecules of air surrounding it to alternately condense and rarefy (pull apart) -> governed by diffusion of air molecules
  • These fluctuations in air pressure travel away from the source as a sound wave at
    approximately 700 miles/hour
  • Something vibrating really slow is a low note and something vibrating very fast is a high note
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144
Q

How do sound waves affect our ears?

A
  • Changes in air pressure from sound waves move the eardrum in and out
  • High amplitude movement will determine how far in or out our eardrum is going
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145
Q

What are the 3 dimensions of sound?

A
  • Loudness
  • Pitch (tone)
  • Timbre
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146
Q

What does the loudness of sound correspond to?

A

Corresponds to the amplitude or intensity of the molecular vibrations

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147
Q

What does the pitch/tone of sound correspond to?

A
  • Corresponds to the frequency of the molecular vibrations
  • Measured in hertz (Hz) or cycles per second
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148
Q

What does the timbre of sound correspond to?

A
  • Corresponds to the complexity of the sound wave
  • We use timbre to help identify the source of the sound wave (through learning processes) -> which instrument made the sound
  • The specific mixture of frequencies that different instruments emit when the same note is played
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149
Q

What’s the pinna?

A
  • The outer ear
  • Sound is funnelled through it
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150
Q

What’s the tympanic membrane?

A
  • The eardrum
  • Separates the outer and middle ear
  • Mechanical amplification device
  • Sounds coming down the ear canal cause the tympanic membrane (the eardrum) to vibrate
151
Q

What are the 3 ossicles (small bones) in the middle ear?

A
  • malleus
  • incus
  • stapes
152
Q

What’s the cochlea?

A
  • The inner ear
  • Fluid-filled
  • Long coiled tube-like structure that contains sensory neurons
153
Q

Describe the process of sound travelling down the ear

A
  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. 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)
154
Q

What happens to the basilar membrane as sound travels in the ear?

A
  • Different parts of it are bent due to variations in air pressure (high frequency air pressure deforms the basilar membrane towards the oval window and low frequency deforms it towards the cochlea)
  • High to medium frequency vibrations cause flexing of different portions of the basilar membrane -> coded in narrow and tight area
  • Low frequency vibrations cause tip of basilar membrane to flex in synchrony with the vibrations -> coded in wide and loose area
  • Ion channels are opened or closed through deforming this membrane
155
Q

What are the 3 longitudinal divisions of the cochlea?

A
  • scala vestibuli
  • scala media
  • scala tympani
156
Q

What’s the receptive organ in the cochlea?

A
  • 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
157
Q

What are the cells that transduce sound called?

A

Hair cells because of their physical appearance

158
Q

What’s cilia?

A
  • Hair-like extensions of hair cells
  • Outer hair cells have cilia that are physically attached to the rigid tectorial membrane
  • Cilia of inner hair cells are not attached to anything. They sway back and forth with the movement of the solution
159
Q

How does sound travel through the cochlea?

A
  1. Sound waves cause the basilar membrane to move relative to the tectorial membrane
  2. This causes hair cell cilia to stretch and bend
  3. The movement of the cilia pulls open ion channels, which changes the membrane potential of hair cells
160
Q

What happens if we delete inner hair cells VS outer hair cells?

A
  • We can delete inner cells and animals become completely deaf (people without these are deaf)
  • If we delete outer hair cells, animals just have bad hearing (people without these have bad hearing)
161
Q

What’s the ratio of inner hair cells VS outer hair cells?

A

There are 3 times more outer hair cells than inner hair cells

162
Q

Which kind of hair cell transmits auditory information to the brain?

A

Inner hair cells

163
Q

How do outer and inner hair cells work together to process sound?

A
  • Outer hair cells contract 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
164
Q

What are tip links?

A
  • Elastic filaments that attach the tip of one cilium to the side of adjacent cilium
  • The cilia of hair cells are connected to each other by tip links
165
Q

What’s the point of attachment of a tip link to a cilium called?

A
  • 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
166
Q

What happens to the tip link and hair cells when there’s very loud sound?

A
  • With very loud sound there is very loud vibration of water in the ear which causes the tip links to break
  • Hair cells can’t transmit auditory information without tip links
  • Tip link breakage generally leads to temporary hearing loss
  • Tip links usually grow back within a few hours
167
Q

How could tip link breakage be a protective measure?

A

Because too much glutamate release onto the cochlear nerve causes permanent cell death (excitotoxicity)

168
Q

What’s the major principle of auditory coding?

A

Different frequencies of sound produce maximal stimulation of hair cells at different points on the basilar membrane

169
Q

What’s place coding?

A
  • Approach to encoding sensory information where different frequencies of sound produce maximal stimulation of hair cells at different points on the basilar membrane
  • 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 coding (Ex: Human speech)
170
Q

What are low frequencies largely encoded by?

A
  • Rate coding
  • It identifies the pitch of low frequency sounds
  • The rate of neurotransmitter release from the hair cells deepest in the cochlea determines the perception of low frequency sounds
  • Placement does not matter only rate of neurotransmitter release
171
Q

What happens to inner hair cells when lesions are conducted on outer hair cells?

A

The responsiveness of inner hair cells to specific sounds is disrupted

172
Q

What does the response to varying frequency threshold look like for inner hair cells?

A

-Inner hair cells will respond to faint sound only if it’s of a specific frequency
- If the sound is louder, cells will respond to frequencies above and below their preferred frequencies
- The wider the frequency range, the more glutamate release

173
Q

How is loudness assessed in the ear?

A

It corresponds to the total number of hair cells that are active and their overall activity levels

174
Q

How is timbre assessed in the ear?

A

Assessing the precise mixture of hair cells that are active throughout the entire cochlea

175
Q

What’s the fundamental frequency of a sound wave?

A
  • The lowest and most intense frequency of a complex sound
  • This frequency is what is most often perceived as sound’s basic pitch
176
Q

What are natural sounds comprised of?

A

Comprised of a fundamental frequency and a collection of overtones

177
Q

What’s overtone?

A

Sound wave frequencies that occurs at integer multiples of the fundamental frequency

178
Q

Describe deafness in individuals

A
  • Generally there’s different issues with inner hair cells (mutations) -> developmental issues
  • For people who are born deaf or develop it, axons are still there (auditory nerves are there)
179
Q

How do hearing aids work?

A
  • Cochlear implants
  • Sticking metal wires and delivering electricity to the cochlea and trigger action potentials in the ear
  • There’s a microphone outside the ear that’s recording sounds which then goes inside the ear to a receiver
  • Typically, 20-24 electrodes are positioned along the length of the cochlea and will stimulate sound
  • This works great for deaf people to hear human speech, but with this implant they usually don’t like music
180
Q

What’s the fundamental frequency of human speech?

A
  • 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
181
Q

How do we detect the source of continuous low-pitched sounds?

A
  • From 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
182
Q

How do we detect the source of high-pitched sounds?

A

By analyzing differences in loudness between the ears

183
Q

How do animals detect the source of sounds?

A
  • 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
184
Q

Describe the process of sound going from the ears to the brain

A
  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 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
  5. This in turn relays the information to the primary auditory cortex in the temporal lobe
185
Q

Why is the primary auditory cortex similar to the basilar membrane?

A
  • Via 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
186
Q

Where is the primary auditory cortex located?

A

In the upper section of the temporal lobe, mostly hidden in the lateral fissure

187
Q

What do the belt and parabelt regions refer to?

A

The auditory association cortex

188
Q

What’s the function of the posterior (dorsal) auditory pathway?

A
  • Involved in sound localization
  • “Where”
189
Q

What’s the anterior (rostral) auditory pathway?

A
  • This pathway goes into the frontal lobe, where analysis of complex sounds occur
  • “What”
190
Q

What happens if you damage your primary auditory cortex?

A

You become deaf

191
Q

What is auditory agnosia caused by?

A

Caused by brain damage in auditory association cortex

192
Q

What’s the function of the auditory association cortex?

A
  • 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)
  • Certain combinations of musical notes can trigger emotions (happy or sad)
193
Q

What’s amusia?

A
  • Amusia is the inability to perceive or produce melodic music
  • 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 usually can’t tell the difference between consonant music (pleasant sounding harmony) and dissonant music (unstable, transitional), even though these sounds might alter their emotional state
194
Q

What’s the vestibular system and where is it located?

A
  • Located in the inner ear beyond the cochlea
  • Detects gravity and angular acceleration of the head from the fluid in ear
  • Maintains upright head position, organizes balance, and corrects eye movements to compensate for head movements
195
Q

What’s a very delicate system?

A

Sense of balance

196
Q

What are vestibular sacs?

A

a set of 2 receptor organs in each inner ear (utricle & saccule) that detect changes in the tilt of head (gravity)

197
Q

What are semicircular canals?

A

3 ring-like, fluid-filled structures that detect changes in head rotation (angular acceleration)

198
Q

What’s the cupula?

A
  • Gelatinous mass found in the ampulla of the semicircular canals
  • Moves in response to the flow of fluid in canals
199
Q

What are the utricle and saccule?

A

They’re in the vestibular sac and respond to the force of gravity and inform the brain about the head’s orientation

200
Q

In mammals, where does the initial transduction and processing of pheromones occur?

A

In the vomeronasal organ and ‘accessory olfactory bulb’ which is inside the nasal cavity

201
Q

How are pheromones detected in mammals?

A

They’re detected by metabotropic vomeronasal receptors

202
Q

Which organisms don’t have functional vomeronasal organs?

A
  • Humans
  • Apes
  • Birds
203
Q

Where do many mammals release their pheromones?

A
  • In their urine
  • Molecules from urine have to be actively sniffed or tasted to be detected
204
Q

Pheromone detection strongly influences what kind of behaviour in mammals?

A

Sexual behaviour

205
Q

What happens if the vomeronasal system is functional in a male mouse VS if the male vomeronasal system is damaged?

A
  • 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
206
Q

What kind of pheromone signalling is most powerful? Female to male or male to female?

A

Female to male

207
Q

What kind of pheromone signalling do females look for in males?

A

Females prefer males that have healthy testosterone levels (vs castrated males)

208
Q

What’s the Lee-Boot Effect?

A

When female mice are housed together (without any male urine present), their estrous cycles slow down and eventually stop

209
Q

What’s the Whitten Effect?

A

Pheromones in the urine of male mice can trigger synchronous estrous cycles in groups of female mice

210
Q

What’s the Vandenbergh Effect?

A

Earlier onset of puberty seen in female animals that are housed with males

211
Q

What’s the Bruce Effect?

A
  • The tendency for female rodents to terminate their pregnancies following exposure to the scent of an unfamiliar male
  • Risk of miscarriage increases
212
Q

Do the different pheromone effects change when exposed to the urine of castrated males?

A

Yes, when only exposed to the urine of castrated males these effects do not occur

213
Q

What’s the difference between menstrual cycle and estrous cycle?

A
  • During menstrual cycle there is bleeding and ovulation is hidden (not obvious to other species and to themselves)
  • During the estrous cycle ovulation and fertility is very obvious to others and herself (relates to changes in behaviour and release of pheromones)
214
Q

How is sleep research conducted?

A
  • It’s conducted in a sleep laboratory
  • Brain activity is measured by attaching electrodes to the scalp to record an electroencephalogram (EEG).
  • Muscle activity is measured by attaching electrodes to the chin to record an electromyogram (EMG).
  • Electrodes are also placed near the eyes to measure eye movements via an electro-oculogram (EOG)
215
Q

What’s the general pattern when people sleep?

A
  • Within the 1st 20 mins you fall into a very deep non-REM sleep
  • At the end of REM (light sleep cycle), you tend to wake up for like 30 secs
  • First half of the night is in very deep sleep (slow-wave sleep)
  • 2nd half of the night is in REM sleep
216
Q

What happens to the body in different stages of sleep?

A
  • In deep sleep, you maintain your posture and balance -> body maintains muscle tone
  • As soon as you enter REM sleep you experience body paralysis (ex: you fall off the chair)
  • During REM sleep eye movements look similar to awake eye movements
217
Q

When does the beta activity occur (related to sleep)?

A
  • Happens when awake
  • Typical of an aroused state
  • It reflects desynchronous neural activity (high frequency, low amplitude oscillations)
218
Q

When does the alpha activity occur (related to sleep)?

A

Typical of awake person in a state of relaxation

219
Q

When does the theta activity occur (related to sleep)?

A

Appears intermittently when people are drowsy, and is prominent during early stages of sleep

220
Q

When does the delta activity occur (related to sleep)?

A
  • Occurs during deepest stages of slow-wave sleep
  • Reflects synchronized low frequency, large amplitude brain activity
221
Q

What’s REM sleep?

A
  • Rapid eye movement sleep (also called paradoxical sleep)
  • 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
222
Q

What’s slow-wave sleep?

A
  • 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
223
Q

What’s a study that was done on REM deprivation and what was found?

A
  • 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
  • Behaviour and physiology of animals changed: they lost their ability to remember things, lost control of hunger, which caused a dramatic stress response
  • We don’t know what REM sleep does because we haven’t found a way of disrupting REM in animals without triggering a stress response (could just be stress related and not REM deprivation related)
224
Q

What’s a study that was done on sleep deprivation and what was found?

A
  • An experimental rat is kept awake because the onset of sleep (detected with EEG) triggers movement of the cage floor
  • It was found that after 2 to 3 weeks of sleep deprivation, the experimental animals begin to lose control of their metabolic processes and body temperature. (They get hot which leads to eating too much). They then hallucinate and have seizures and then die
225
Q

What are 2 components of sleep that are vital?

A

REM and slow wave sleep

226
Q

What are some effects of lack of sleep?

A
  • Start to exhibit delayed reaction times and poor judgment (as measured on performance in cognitive tests)
  • Increases in stress hormones, mood swings, and impulsive behavior
  • Exhibit worse learning and memory
  • Increase propensity for weight gain (people tend to eat more especially fast food), migraines, hallucinations, dementia, seizures, and death
  • Sleep debt is created that must be repaid
  • Microsleep states often appear
  • Sleep disruptions often precede and exacerbate mental illnesses
227
Q

What are microsleep states?

A
  • They 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
  • Ex: occurs a lot where truck drivers fall asleep at the wheel
228
Q

True or False? Someone can take caffeine and meth and stay awake for as long as they want

A

False. You need sleep and can’t force yourself to stay awake

229
Q

How do dolphins manage to get sleep when they’re constantly awake?

A
  • Dolphins and some fish have to keep swimming so they never let the entire brain sleep at the same time
  • Their version of sleep alternates between the two cerebral hemispheres
  • In some fish it’s not obvious that one side is sleeping because of their hindbrain
230
Q

What’s the difference between infants and adults for the amount of REM sleep they have?

A
  • 50% of human infant sleep is REM sleep
  • 25% of human adult sleep is REM sleep
231
Q

What are differences of sleep patterns that can occur between different species?

A
  • Amount of sleep
  • Ratio of REM to non-REM sleep
  • Length of sleep cycles (average time between two REM events
232
Q

What’s the correlation found between sleep and weight in animals?

A
  • The larger the animal is, the less sleep they need
  • Found especially in herbivores and less in carnivores
233
Q

What’s basal metabolic weight?

A

How many calories you burn by just sitting not doing anything

234
Q

What are the correlations between metabolic rate and body weight?

A
  • While overall metabolic rate increases as mass increases, metabolic rate per pound (or per cell) decreases as mass increases
  • As you get bigger, each of your cells has to work less hard (make less sugar and digest less ATP overall)
235
Q

What are economies of scale and what kind of animals benefit from it?

A
  • 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
236
Q

What are the 3 main theories behind why animals sleep?

A
  1. To recover from physical or mental exertion -> doesn’t occur to be the case for our population since the amount of sleep people get does not correlate very well with how much or how little they exercise or study
  2. Brain Processing (learning and memory) -> the amount of slow-wave and REM sleep people get correlates with improvements in declarative and procedural memory -> we sleep to fix neural and synaptic activity in the brain
  3. Waste removal -> critical for a process that benefits from economies of scale (nutrient transport or waste removal systems)
237
Q

How does sleep improve learning and memory?

A
  • Sleep gives the brain an opportunity to reorganize data and archive memories, which perhaps cannot be done efficiently while awake
  • 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)
    Ex: computer updates have to be done when turned off
238
Q

How are memories worked on in different stages of sleep?

A
  • During deep sleep we readjust all the declarative memories
  • When we go up to REM sleep, we readjust motor memories (procedural memory processing)
239
Q

What’s the most popular sleep theory these days?

A
  • The waste removal theory
  • It’s been reported that the concentration of certain proteins in the brain increases across periods of wakefulness and decreases across periods of sleep
  • Recent research has shown that the clearance of proteins and waste products from the brain is almost nonexistent during wakefulness but really high during sleep
  • Waste clearance systems in the brain benefit from economies of scale
240
Q

What happens to glial cells in the brain (astrocytes) during sleep?

A
  • They seem to lose water and shrink in size, which increases the total volume of interstitial space (extracellular solution), which promotes diffusion of cerebrospinal fluid through the brain and clears away waste
241
Q

What’s the glymphatic system?

A

Process where cerebrospinal fluid removes excess proteins and other waste from the interstitial space of the brain

242
Q

What’s the lymphatic system?

A

Process where cellular waste is cleared away everywhere else in the body

243
Q

What’s a circadian rhythm?

A
  • The daily change in behaviour and physiological processes that follows a cycle of approximately 24 hours
  • When sunlight gets disrupted, we adapt our cycles with biological clocks
  • It’s maintained by the production of several genes and two interlocking feedback loops
244
Q

What’s the suprachiasmatic nucleus (SCN)?

A
  • In the hypothalamus
  • It regulates sleep-wake cycles
  • It receives a direct input from the retina
245
Q

What do lesions to the suprachiasmatic nucleus (SCN) do?

A
  • They dramatically alter and disorganize circadian rhythms (such as sleep-wake cycles and hormone secretions)
  • Animals still sleep the same amount though
246
Q

What’s advanced sleep phase syndrome?

A

Mutation of a gene called per2 (period 2) causes a 4-hour advance in the biological clock – strong desire to fall asleep at 7pm and wake up at 4am

247
Q

What’s delayed sleep phase syndrome?

A

Mutation of a gene called per3 causes a 4-hour delay in rhythms of sleep – strong desire to fall asleep at 2am and wake up at 11am

248
Q

Which molecule is related to the sleep molecule hypothesis?

A
  • Adenosine molecule (part of ATP)
  • 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 signaling throughout the brain
  • Determines homeostatic need for sleep
249
Q

What’s an adenosine receptor antagonist?

A

Caffeine as it promotes arousal

250
Q

What are signaling molecules that show increased activity during periods of arousal, alertness, and wakefulness and decreased activity during slow-wave sleep (wake promoting molecules)?

A
  • Serotonin
  • Norepinephrine
  • Acetylcholine
  • Orexin
  • Histamine
251
Q

What kind of receptor blockers often cause drowsiness?

A

Histamine (antihistamine)

252
Q

What are Orexin and Histamine?

A

Neuropeptides that are released by neurons in the hypothalamus

253
Q

What does norepinephrine neuron activity correlate with?

A

It positively correlates with focus and attention

254
Q

What does serotonin neuron activity correlate with?

A
  • It positively correlates with cortical arousal (as measured by EEG)
  • Drugs that increase serotonin signaling tend to suppress aspects of REM sleep (without affecting memory)
255
Q

Neurons in what area of the hypothalamus promote sleep?

A

Neurons in the ventral lateral preoptic area (vlPOA)

256
Q

What happens when there’s electrical stimulation VS lesions of the ventral lateral preoptic area (vlPOA)?

A

Electrical stimulation: causes drowsiness and sometimes immediate sleep
Lesions: suppress sleep and cause insomnia

257
Q

Explain the flip-flop circuit of the the ventral lateral preoptic area (vlPOA)

A
  • vlPOA neurons inhibit wake-promoting neurons. But this area receives inhibitory inputs from the same regions it inhibits.
  • Both regions can’t 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
258
Q

How are sleep-promoting vlPOA neurons activated?

A

By adenosine signaling

259
Q

Describe the function of Orexin neurons

A
  • Orexin neuron activity promotes wakefulness
  • Motivation to remain awake activates orexin neurons
  • Most forms of narcolepsy are associated with the absence of orexin neurons
260
Q

What’s Narcolepsy?

A
  • Rare sleep disorder characterized by periods of excessive daytime sleepiness and irresistible urges to sleep
  • Related to the death of orexin neurons in the hypothalamus, which seem to be attacked by the person’s own immune system, usually during adolescence or young adulthood
  • Can experience sleep paralysis and cataplexy
261
Q

What’s sleep paralysis?

A
  • When REM-associated paralysis occurs just before a person falls asleep or just after they wake up
  • Often accompanied by vivid, dream-like hallucinations
262
Q

What’s cataplexy?

A
  • Intrusion of REM-like state
  • Complete muscle paralysis suddenly occurs when someone is awake
  • Typically precipitated by strong emotional reactions or sudden physical effort (e.g., laughter, anger, excitability)
263
Q

What’s the difference in sleep patterns between a person with orexin neurons and one without?

A
  • When the average person goes to sleep, they start off with non-REM sleep and later fall into REM
  • People without orexin neurons seem to go into REM sleep right away
264
Q

What seems to cause sleep disorders?

A

A mix up with flip flop sleep circuits

265
Q

What’s Fatal Familial Insomnia & Sporadic Fatal Insomnia?

A
  • A very rare disease that involves progressively worseninginsomnia, which leads to hallucinations, delirium, and confusional states
  • Lose ability to fall asleep
  • Typically inherited but can also develop spontaneously
  • Has no known cure and the average survival span after the onset of symptoms is 18 months
  • If people can’t sleep they can go to the emergency room and get general anesthesia to be put to sleep, but general anesthesia can be fatal if used too much
266
Q

What are non-REM parasomnias and what are examples of them?

A
  • Sleep disorders that occur during non-REM sleep or during transitions out of sleep
  • Sleepwalking, Sleep-talking, Sleep-groaning, Sleep-crying, Sleep-eating, Sleep-masturbating, Sleep-teeth grinding
  • Sleep terrors
267
Q

What’s REM sleep behavior disorder?

A
  • 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
  • Often associated with Parkinson’s disease
  • Can be very violent and so is dangerous
268
Q

What’s sexual dimorphism?

A
  • Condition where the 2 sexes of the same species exhibit different characteristics beyond the differences in their sexual organs (differences in size, weight, color, behavior and cognition)
  • Associated with genetic and hormonal differences, both before and after birth
269
Q

What are sexual dimorphic behaviours?

A
  • Behaviors 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 are reproductive behaviors
  • The brain gives rise to sexual dimorphic behaviors because it is a sexually dimorphic organ. The size and interconnectivity of different brain regions vary according to sex.
  • For human behaviour, there are differences between the sexes (talents, temperaments, and interests)
  • Power of socialization and biological functions serve these sexual dimorphic behaviours
  • Sex differences that show differences in reactions to treatments and diff prevalence in mental illness
270
Q

What’s the difference between sexual orientation and sexual identity?

A
  • Sexual orientation refers to one’s enduring romantic or sexual attractions
  • Sexual identity refers to an individual’s conception of themselves in terms of whether they identify (or not) with a sexual orientation
271
Q

What does sexual reproduction involve?

A

The fusion of specialized cells known as gametes (one from each parent) to form offspring that inherit traits from each parent

272
Q

What are gonads?

A
  • Ovaries or testes
  • They make reproductive cells called gametes, which are either ova (egg cells) or sperm
273
Q

How many chromosomes do the cells in our body have?

A
  • They have 46 chromosomes…half from mom half from dad (23 pairs)
  • X & Y being the 23rd chromosomes
274
Q

In humans, what are the five factors present at birth that determine biological sex?

A

Sex chromosomes: XX or XY
Sex hormones: androgen signaling
Internal reproductive anatomy
External anatomy
Gonads: testes or ovaries
- Internal/external anatomy and gonads being the categories of sex organs

275
Q

What are Undifferentiated gonads?

A

Embryonic precursor of ovaries/testes

276
Q

What’s the Mullerian system?

A

Embryonic precursors of female internal sex organs

277
Q

What’s the Wolffian system?

A
  • Embryonic precursors of male internal sex organs
278
Q

When do sex organs develop?

A
  • During 2nd month of gestation, the undifferentiated gonads typically develop into ovaries or testes
  • During 3rd month of gestation, typically either the Müllerian or Wolffian system develops while the other withers away
279
Q

What’s the SRY gene?

A
  • Gene normally located on the Y chromosome encodes a protein that causes undifferentiated fetal gonads to develop into testes which start releasing testosterone
  • This gene overpowers XX-ovary instructions, so XXY individuals develop testes
280
Q

What are androgens?

A

Male sex hormones

281
Q

When do ovaries release signalling molecules?

A
  • After puberty
  • Puberty is triggered by hormones released from gonads (ovaries or testes)
282
Q

What’s Turner syndrome?

A

When you only have one sex chromosome (X0) so you’re born without testes or ovaries

283
Q

What’s Swyer syndrome?

A
  • When you are XY but have a bad SRY gene so the gonads never come out
  • These people develop into healthy females because there is no hormone release from the gonads … won’t go through puberty
284
Q

What happens to people who do not develop gonads?

A

They’re infertile and don’t naturally experience puberty

285
Q

What happens to people who can have two (or more) X chromosomes as well as the SRY gene (e.g., XXY or XXXY)?

A

They typically develop as males and are often infertile with small testes and have trouble growing a beard

286
Q

What happens to people with insufficient anti-Müllerian hormone signaling?

A
  • There will be insufficient anatomical defeminization: both male and female internal sex organs will develop and get tangled together
  • There is often functional external male genitalia
287
Q

What happens to people with Androgen insensitivity syndrome?

A
  • Results in anatomical defeminization with partial or no masculinization.
  • In severe cases, no internal sex organs develop so 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
288
Q

What are examples of activational effects of sex hormones?

A
  • Production of sperm, ovulation, and general horniness
289
Q

What part of the brain controls puberty?

A

The hypothalamus

290
Q

What’s Kisspeptin?

A

Neuropeptide produced by neurons in the hypothalamus that initiates puberty and maintains reproductive ability by triggering release of gonadotropin-releasing hormone

291
Q

What will happen if men take a gonadotropin-releasing hormone antagonist?

A

They will not show testicular release of androgens and have a decrease in sexual interest and intercourse

292
Q

What’s estradiol?

A

The principal estrogen of many mammals, including humans

293
Q

Menstrual and estrous cycles are controlled by what two ovarian hormones?

A

Estradiol and Progesterone

294
Q

What’s congenital adrenal hyperplasia (CAH)?

A
  • Condition present at birth for females where excess androgen signaling can cause some degree of masculinization of either the body or brain or both
  • Depending on the amount of androgen signaling during development, sex organs can become slightly masculinized (e.g., enlarged clitoris, partially fused labia)
  • Brain anatomy and function can also be masculinized. Females with CAH have a higher likelihood of identifying as a man and being sexual attracted to women in comparison to other females
  • Could explain homosexuality and transgenderism
295
Q

What’s the Ventromedial nucleus of hypothalamus (VMH)?

A

Large nucleus in the hypothalamus that plays essential role in female sexual behavior

296
Q

What animals are sexually attracted to relates to activation of which part of the brain?

A

The medial amygdala

297
Q

What’s the Medial Preoptic Area (mPOA)?

A
  • Nucleus in the anterior hypothalamus that plays essential role in male sexual behavior
  • Lesioning the mPOA of female rats does not affect their sexual behavior, but it does cause them to ignore their offspring
298
Q

The formation of pair bonds seems to relate to what two peptides in brain?

A
  • Vasopressin and Oxytocin
  • Released as neuropeptides in the brain and as hormones in the blood
  • Levels of them are elevated during sex, childbirth, and breastfeeding
  • If we block vasopressin and oxytocin -> they won’t form pair bonds
  • If we activate vasopressin and oxytocin -> they will form pair bonds
299
Q

What’s the ventral forebrain and nucleus incumbus?

A

Areas controlling motivational processes -> works with pairing up and drug addiction

300
Q

Which part of the brain works for sex and aggression in animals?

A

The medial amygdala

301
Q

How does a patient with bilateral amygdala damage react when shown photographs of faces?

A
  • They usually don’t look at the eyes
    -They can be trained to recognize emotion through looking at the eyes but have to be reminded to do so everytime
302
Q

How do some people lack the ability to feel fear or recognize it on the face of other people?

A

Lack of amygdala on one side of the brain

303
Q

What’s the role of Ventromedial Prefrontal Cortex (vmPFC)?

A
  • Involved in regulating expressions of emotions; usually has an inhibitory influence
  • When conditioned fear responses are extinguished, 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. They act more childlike
  • People with a healthy vmPFC can usually calm themselves when they get frustrated and thus suppress emotional outbursts
304
Q

Why are children bad at regulating their emotions?

A

Because their prefrontal cortex has not finished being myelinated

305
Q

What’s homeostasis?

A

Process by which body’s substances and characteristics (such as temperature and glucose level) are maintained at their optimal level

306
Q

What’s the Satiety mechanism?

A
  • Brain mechanism that causes cessation of hunger or thirst, produced by adequate and available supplies of nutrients or water
  • Preemptive measure
307
Q

What’s volumetric thirst?

A

When there’s not enough blood circulating in the body (hypovolemia)

308
Q

What’s osmometric thirst?

A

there is too much salt in the extracellular fluid of the body, which causes cells to lose water and shrink in size

309
Q

Low blood flow causes the kidneys to release what?

A

Renin, which triggers a hormone signaling cascade that promotes thirst, among other things

310
Q

The feeling of thirst is related to the activation of what?

A

The hypothalamic neurons near the anteroventral tip of the third ventricle (the AV3V region), where the blood brain barrier is weak

311
Q

What’s tonicity?

A
  • Refers to the relative concentration of dissolved solutes (e.g., salt) on either side of a membrane that is permeable to water
  • It is used to describe the direction and amount of water flow across the membrane (i.e., osmosis
312
Q

What’s an Isotonic solution?

A

Similar solute concentrations are present inside and outside the cell. The cell will neither gain nor lose water

313
Q

What’s a Hypotonic solution?

A

solute is less concentrated outside the cell than in, so water will enter the cell

314
Q

What’s a hypertonic solution?

A
  • solute is more concentrated outside the cell than in, so water will leave the cell
  • cause cellular dehydration
315
Q

Food mostly consists of what?

A
  • Sugars (carbohydrates)
  • Lipids (triglycerides)
  • Amino acids (proteins)
316
Q

What happens when blood glucose levels are high in the pancreas?

A

The pancreas releases insulin, which causes liver and muscle cells to store glucose as glycogen

317
Q

What happens when blood glucose levels are low in the pancreas?

A

The pancreas releases glucagon, which causes liver and muscle cells to convert glycogen back into glucose

318
Q

What happens when there’s an absence of insulin in the body?

A

Cells outside the brain must break down fatty acids to create the glucose they need for energy

319
Q

What kind of signalling promotes the breakdown of triglycerides into fatty acids?

A

Glucagon signalling

320
Q

What are the 2 phases of digestion?

A
  • Absorptive phase: when digestive system contains food
  • Fasting phase: when digestive system is empty
321
Q

What’s the peptide hormone that’s released by an empty stomach (or, more accurately, an empty duodenum) ?

A
  • Ghrelin
  • Increases with hunger and falls with satiation
  • Ghrelin levels tend to rise before every meal and during sleep
  • Produced by neurons in the brain
322
Q

Does repeated administration of CCK and PYY to healthy people make them lose weight?

A
  • Does not reliably cause sustained weight loss
  • They can decrease meal size, but there are typically increases in meal frequency
323
Q

What does the liver measure?

A

Levels of glucose and fatty acid levels in the blood

324
Q

What does the pancreas measure?

A

It measures blood-glucose level

325
Q

The detection of insulin by neurons in the hypothalamus reduces what?

A

Feelings of hunger

326
Q

Exogenous administration of what hormone temporarily decreases meal size in healthy people?

A

Leptin
- It encourages weightloss

327
Q

What are the hedonic aspects of hunger?

A
  • They refer to the motivational and reinforcing properties of food, which fluctuate in accordance with hunger and available energy
  • Hunger increases the rewarding and reinforcing value of food
  • Satiety reduces the rewarding and reinforcing value of food
328
Q

Which neuropeptides released by hypothalamic neurons all play an important role in regulating hunger, particularly the hedonic aspects of hunger?

A

NPY, orexin, and MCH (melanin-concentrating hormone)

329
Q

What’s the difference between AGRP/NPY neurons and POMC/a-MSH neurons?

A
  • AGRP/NPY neurons promote hunger. They’re inhibited by leptin and activated by ghrelin
  • POMC/a-MSH neurons inhibit hunger. They’re activated by leptin and inhibited by ghrelin
  • These 2 types of neurons’ sensitivity to leptin seems to have a profound influence on how much fat an animal thinks it is necessary to have for glucose storage
330
Q

What’s Prader-Willi syndrome?

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 oxytocin-containing neurons in the PVN.
  • Oxytocin neurons either don’t develop or don’t survive in the PVN
  • People are born with very low muscle mass and have little interest in eating
  • Between 2 and 8 years old, these people develop a heightened, permanent and painful sensation of hunger, a feeling of starving to death
  • They 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
331
Q

What is leptin resistance related to and what does it cause?

A
  • Overweight populations
    Causes:
  • A reduction in leptin’s ability to cross the blood-brain barrier
  • A reduction in the neuronal response to leptin signalling
  • A reduction in the downstream consequences of leptin-signalling neurons
332
Q

What aspect of emotions is processed in the neocortex?

A
  • Stream of thought
  • Cognitively thinking about emotions and making your face artificially express specific emotions (like when people tell you to smile to look happy or you pretend to be sad)
333
Q

What aspect of emotions is processed in the limbic system and most prominently in the amygdala?

A
  • Stream of feeling
  • Raw reflexive response to certain stimuli
334
Q

What’s volitional facial paresis?

A
  • A condition where people are unable to voluntarily control their facial muscles, but they can express genuine emotion with the same muscles
  • Caused by damage to face region of primary motor cortex or its subcortical connections
335
Q

Whats emotional facial paresis?

A
  • A condition where people are unable to express genuine emotion with their facial muscles, but they can voluntarily control their facial muscles
  • Caused by damage around insular cortex or parts of the thalamus
336
Q

What’s the theory of emotion?

A
  1. Perception of the emotion-eliciting event (e.g., see a bear)
  2. Subjective feelings of emotion (e.g., fear)
  3. Behavioral and physiological responses (e.g., trembling, sweating and running away)
337
Q

Where are the hippocampus and amygdala located in the brain?

A

In the temporal lobe

338
Q

What’s the James-Lange Theory of emotion?

A
  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 from these changes in the peripheral nervous system which, in turn, produces the subjective feelings of emotion.
339
Q

What would interfering with muscular movement associated with emotion do?

A

It would decrease people’s ability to experience that emotion

340
Q

What happens to a patient who received a bilateral amygdalectomy to treat a severe seizure?

A
  • She doesn’t experience fear, but she can generate artificial expressions of emotion (even fear) without problem
  • She cannot identify expressions of fear in photos of faces, even her own
341
Q

Which cerebral hemisphere is related to emotional processing?

A

Right cerebral hemisphere

342
Q

What are mirror neurons?

A
  • 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
343
Q

Beyond the amygdala, what are brain areas that activate when we see emotional faces?

A

The somatosensory cortex, insular cortex, premotor cortex, and anterior cingulate cortex

344
Q

What’s a trait of people with low levels of serotonin?

A
  • impulsivity
  • aggression
  • irritability
345
Q

When does thirst appear?

A
  1. When not enough blood circulating in the body (volumetric thirst)

Or

  1. When there’s too much salt in the extracellular fluid of the body, which causes cells to lose water and shrink in size (osmometric thirst)
346
Q

How do cells internalize glucose?

A
  • With a glucose transporter
  • Cells outside the brain use a glucose transporter that requires insulin to be functional
  • This means that cells outside the brain can only use glucose when there’s an excess amount of it in the body (signaled by insulin)
  • Cells within the brain have an additional glucose transporter that works in the absence of insulin, so brain cells can always internalize sugar
347
Q

What’s Glycogen?

A
  • Polysaccharide often referred to as animal starch
  • Stored in liver and muscle
  • Constitutes the short-term store of nutrients
348
Q

What’s Insulin?

A

Pancreatic hormone that facilitates:
1) conversion of glucose into glycogen
2) entry of glucose and amino acids into cells of the body
3) transport of fats into adipose tissue

349
Q

What’s Glucagon?

A

Pancreatic hormone that promotes
1) conversion of liver glycogen into glucose
2) conversion of adipose triglycerides into fatty acids

350
Q

What kind of signalling promotes the storage of fatty acids as triglycerides in adipose tissue (fat cells)?

A

Insulin signaling

351
Q

What’s a triglyceride?

A
  • Form of fat storage in adipose cells (fat cells)
  • Constitutes the long-term store of nutrients
  • Consists of molecule of glycerol joined with three fatty acids
352
Q

What’s Glycerol?

A
  • Substance (also called glycerine) derived from breakdown of triglycerides, along with fatty acids
  • Can be converted by liver into glucose
353
Q

What’s a fatty acid?

A
  • Substance derived from breakdown of triglycerides, along with glycerol
  • Can be metabolized into sugars by most cells of body except for brain
354
Q

What happens when there’s a decrease in blood glucose?

A
  • Causes the pancreas to stop secreting insulin and start secreting glucagon
  • The absence of insulin means that most cells of body can no longer use glucose
  • Thus, all glucose present in blood is reserved for the central nervous system
355
Q

What does exogenous administration of ghrelin do?

A

Increases hunger and food intake

356
Q

What are CCK, PYY, and GLP-1?

A
  • Satiety-related peptides
  • Secreted by the duodenum in response to food ingestion in proportion to the calories ingested
  • These and other satiety-related peptides correlate with feelings of fullness and inhibit food intake, but the effects are typically short lived
  • These signaling molecules mostly regulate digestive processes
    E.g., CCK causes the gallbladder to release digestive enzymes into the duodenum, and GLP-1 regulates insulin secretion from the pancreas
357
Q

How does the liver signal satiety?

A

Through the 10th cranial nerve (the vagus nerve)

358
Q

What’s leptin?

A
  • 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
  • This leptin provides a negative homeostatic feedback signal that decreases hunger
  • The more fat cells in the body, the more leptin levels in the blood
  • Leptin goes into the brain and changes all the neuron sensitivity to satiety
359
Q

What’s hypoglycemia (glucoprivation)?

A
  • Dramatic fall in amount of glucose available to cells (detected in liver and brainstem)
  • Can be caused by lack of sugar, excess insulin signaling, or by drugs that inhibit glucose metabolism
  • When it senses that there’s not enough glucose, it launches an emergency cascade of effects:
    1. Suppresses insulin secretion to keep sugar in the blood
    2. Triggers glucose production in the liver
    3. Slows energy expenditure (basal metabolic rate) and halts growth and reproduction related systems
    4. Promotes a potent and sustained feeling of hunger
360
Q

What’s lipoprivation?

A
  • Dramatic fall in level of fatty acids available to cells (detected in liver and brain)
  • Usually caused by drugs that inhibit fatty acid metabolism, but it can also relate to too little body fat
  • Dangerously low levels of body fat (signaled by insufficient leptin) trigger the same emergency feeding circuits as dangerously low levels of glucose
361
Q

What can excess insulin trigger?

A

Hypoglycemia and intense hunger, because it causes glucose to be stored in muscle tissue and as fat in adipose cells

362
Q

After several days of eating a cafeteria-style diet (high fat, high sugar), inflammation has been observed in what part of the brain of rodents?

A
  • In the hypothalamic arcuate nucleus of rodents
  • This results in a decreased sensitivity to leptin
  • These animals require more leptin in the blood (more fat cells) to maintain their energy homeostatic set point
363
Q

What region of the brain is thought to play a large role in low leptin-induced emergency feeding?

A

Paraventricular Nucleus (PVN) of the Hypothalamus

364
Q

What’s the paraventricular nucleus (PVN) of the Hypothalamus?

A
  • It contains oxytocin neurons, whose activity signals that body has enough leptin (fat) and inhibits hunger
  • If PVN neurons have a low firing rate, below some threshold, animals will feel intense hunger
  • Excess activity of PVN neurons does not prevent feeding triggered by other parts of the circuitry
365
Q

What’s the arcuate nucleus of the hypothalamus?

A
  • Nucleus in base of hypothalamus that contains neurons highly sensitive to circulating levels of leptin
  • Contains AGRP/NPY neurons and POMC/a-MSH neurons, which are involved in feeding and metabolic rate
366
Q

What does leptin signaling do throughout the body?

A
  • Decreases food intake and increases metabolic rate by acting on leptin receptors located throughout the brain
  • In the arcuate nucleus of the hypothalamus, leptin signaling inhibits AGRP/NPY neurons and activates POMC/a-MSH neurons, which both strongly regulate hunger
  • Leptin signaling also makes neurons more sensitive to satiety peptides such as CCK and less sensitive to hunger peptides such as ghrelin
367
Q

What’s hyperglycemia and what are its effects?

A
  • Disruptions in insulin signaling cause high blood sugar (hyperglycemia), because sugar is not being converted into glycogen or fat
  • If left untreated, this causes ongoing weight loss and loss of body fat
  • The resulting drop in leptin signaling can initiate intense hunger, even if the person is hyperglycemic (too much sugar in blood)
  • This used to happen to diabetics and often led to death before insulin treatments were discovered 100 years ago
368
Q

Neural activity in what part of the brain is directly related to thirst?

A

Anterior cingulate cortex

369
Q

Why are you usually less thirsty when you drink cold water as opposed to room temp water?

A

Cold sensors in the mouth and sensory fibers in the stomach are part of the rapid satiety feedback mechanism

370
Q

What are osmoreceptors?

A
  • Neurons that detect changes in cell size, which corresponds to interstitial solute concentration
  • The membrane potential and release of neurotransmitter from osmoreceptor cells relates to the volume of these cells
371
Q

There is a small correlation between risky behaviour, impulsive aggression and low levels of what molecule?

A
  • Serotonin metabolite 5-HIAA
  • In humans, low cerebrospinal 5-HIAA has been associated with aggression and antisocial behavior, including assault, arson, murder, and child beating
  • Drugs that increase serotonin signaling, such as SSRIs like Prozac, tend to decrease irritability and aggressiveness
  • Animals with low levels of serotonin 5-HIAA in the brain usually died younger -> they often died from attacks from others monkeys, they are risk takers
372
Q

What does damage to the Ventromedial Prefrontal Cortex (vmPFC) do?

A
  • Can severely weaken behavioral control and impair decision-making
  • These impairments appear to be a consequence of emotional dysregulation
  • Doesn’t damage cognitive skills
  • Tend to promote nonmoral behaviour
  • Don’t seem to be taking emotions into consideration that much
373
Q

The raw feeling of emotion coincides with what other types of responses?

A
  • Behavioral responses: consists of muscular movements (facial expressions, body language, choreographed movements)
  • Autonomic responses: (signaling through peripheral nervous system) facilitate fight or flight behaviors and provide quick mobilization of energy for vigorous movement
  • Hormonal responses (signaling through blood) reinforce the autonomic responses
374
Q

Patients with damage to primary visual cortex or visual association cortex may have no conscious awareness of looking at a person’s face, but what do they do?

A

They still show amygdala activity in response to viewing faces and often mimic the presented facial reaction (happy or fearful face)