Midterm #2 Flashcards
Sensation
Refers to how cells of the nervous system detect stimuli in the environment (such as light, sound, heat, etc.), and how they transducer (convert) these signals into a change in membrane potential and neurotransmitter release.
Perception
Refers to the conscious experience and interpretation of sensory information
Sensory neurons
Specialized cells that detect a specific category of physical events, such as: the presence of specific molecules (smell, taste, nausea, pain), the presence or absence of physical pressure
(touch, stretch, vibration), the temperature (heat, cold, pain), the pH of a liquid (sour taste, suffocation, pain), electromagnetic radiation (vision).
Sensory Transduction
Sensory neurons have specialized receptors that transduce sensory stimuli into a change in membrane potential. Come in all shapes and sizes. Many sensory neurons do not have axons or action potentials, but they all release neurotransmitter. Sensory neurons that do not have action potentials release neurotransmitter in a graded fashion, dependent on their membrane potential. The more depolarized they are, the more neurotransmitter they release.
Photoreceptor cells
The sensory neurons responsible for vision. These cells transduce the electromagnetic energy of visible light into a change in membrane potential, which affects how much neurotransmitter they release. These cells do not have action potentials.
Opsins
Light-sensitive proteins. The opsins in photoreceptor cells are metabotropic receptors. They are only sensitive to light because they bind a molecule of retinal, which changes shape in response to light. The change in the shape of retinal is what activates this metabotropic receptor.
Retinal
Small molecule (synthesized from vitamin A) that attaches to the opsin proteins in the photoreceptor cells in our eyes. The retinal molecule is technically what absorbs the electromagnetic energy of visible light that allows us to see.
The two configurations of the retinal molecule
When retinal absorbs a wavelength of visible light, it activates the opsin protein (a metabotropic receptor). This launches an intracellular G protein signalling cascade that changes the membrane potential of the photoreceptor cell, affecting how much neurotransmitter it releases.
4 types of photoreceptor cells that contribute to vision and their metabotropic opsin protein
- Red cone cells express the red cone opsin.
- Green cone cells express the green cone opsin.
- Blue cone cells express the blue cone opsin
- Rod cells express the rhodopsin opsin. (The last to evolve; 100 times more sensitive to light than cone cells).
Cone Photoreceptors: Trichromatic Coding
Blue cone opsins are most sensitive to short wavelengths of light. Green cone opsins are most sensitive to medium wavelengths of light. Red cone opsins are most sensitive to long wavelengths of light.
Color perception is a function of the relative rates of activity across the three types of cone cells (i.e. colors are discriminated by the ration of activity across these cells.)
Trichromatic Coding
The key consideration for our brain for identifying color is how much each type of cone cell is activated relative to its maximum level. Each color of the rainbow corresponds to a particular pattern of activation across the three types of cones cells.
How is yellow light created
When red and green light bulbs are so close together that our eyes can’t differentiate them, the color looks yellow to us. Green light (530nm) activates the green cone opsin more than the red cone opsin. Red light (680nm) activates the red cone opsin more than the green cone opsin. The combination of red and green light causes the red and green cone opsin to be activated at similar amounts, which is what happens with yellow light (580nm).
Additive Color (Light)
Primary colours of light: Green, Red, Blue. Combine to make yellow, cyan, magenta. Sunlight is white light, since it contains an equal mixture of all the colors.
Our perception of light and colour has three dimensions to it
- Brightness - intensity (luminance, amount)
- Saturation - purity (in terms of wavelength mixture)
- Hue - dominant wavelength (colour)
Perceptual Dimensions of colour & light
If brightness is zero, the image is completely black. Hue and saturation have no impact without brightness. If there is (bright) light, the next question is whether the light is saturated with a particular wavelength (colour). If saturation is 0% then you are in the middle of the colour cone where there is an equal contribution from all visible wavelengths. An image with 0% saturation is grayscale (black and white), because all wavelengths are present in equal amounts. If saturation is >0%, the hue indicates the colour that the light is saturated with.
Protanopia
Absence of the red cone opsin (1% of males). People with this condition have trouble distinguishing colours in the green-yellow-red spectrum. Visual acuity is normal because red cone cells switch to using the green cone opsin. Simple mutations of the red cone opsin price less pronounced deficits in colour vision.
Deuteranopia
Absence of the green cone poison (1% of males). People with this condition have trouble distinguishing colours in the green-yellow-red spectrum. Visual acuity is normal because green cone cells switch to using the red cone opsin. Simple mutations of the green cone opsin (6% of males) produce less pronounced deficits in colour vision.
Tritanopia
Absence of the blue cone opsin (1% of the population). Blue cone cells do not compensate for this in any way, but since the blue cone opsin is no that sensitive to light anyway, visual acuity is not noticeably affected).
Visible light
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 & 4 cone cells).
The cornea
The outer, front layer of the eye. It focuses incoming light a fixed amount.
The conjunctiva
Is a mucous membranes that line the eyelid.
The sclera
Is opaque and does not permit entry of light.
The iris
A ring of muscle. The contraction and relaxation of this muscle determine the size of the pupil, which determines how much light will enter the eye.
The lens
Consists of several transparent layers. We change the shape of this lens to focus near versus far, a process known as accommodation.
Retina
The interior lining (furthest back part) of the eye is the retina. Photoreceptor cells are located in the furthest back layer of the retina.
Vitreous humor
Light passes through the lens and crosses the vitreous humor, a clear, gelatinous fluid.
Fovea
The central region of the retina is called the fovea. It primarily contains cone cells.
The periphery of the retina
Only contains rod cells
The optic disk
Where blood vessels enter and leave the eye. It is also where the optic nerve exits the eye, carrying visual information to the brain. There are no photoreceptors in this spot, so it is a blind spot.
Saccadic eye movements
Our eyes scan a scene by making saccadic eye movements - rapid, jerky shifts in gaze from one point to another.
Pursuit movements
When we maintain focus on an object that is moving (relative to us). This is the only time our eyes appear to calm down and move smoothly and slowly.
Orbits
Eyes are suspended in bony sockets in the front of the skull called orbits.
The sclera
The tough, outer white of the eye. Six extra ocular muscles are attached to the sclera. These muscles rotate the eye and hold it in place.
Organization of the retina
Visual inforamtion propagates from photoreceptor cells –> bipolar cells –> retinal ganglion cells –> brain. When light enters our eyes, it must pass through each of the cell layers in the retina before it can reach the opsin proteins in photoreceptor cells. There does not seem to be a good reason for this award arrangement.
Retina Fovea
In fovea, there is an equal number of photoreceptor cells, bipolar cells, and retinal ganglion cells. This means there is no compression of information. The fovea is the only part of our retina where our visual acuity is good enough to read text (20/20 vision). And the photoreceptor cells in our fovea are mostly cone cells, which support colour vision, so the fovea supports high resolution, colour vision. Fovea supports high resolution colour Vision but only when there is sufficient amount of light. At night, the moon must be at least half full for us to see in colour.
Periphery
Outside the fovea (in the periphery of retina), there is a massive compression (averaging) of information, since there are 100x more photoreceptor cells than retinal ganglion cells. Our visual acuity in peripheral vision is about 20/200, which is quite blurry. It is also grey scale. We can make out general shapes but not details. Yet, the periphery contains a high density of rod cells, which are sensitive to light, allowing us to easily. detect dim light and movements of light. While the peripheral vision is sensitive to dim light, it only provides low resolution grayscale images. What we see in peripheral vision 20 feet away is as detailed as what we see in our fovea 200 feet away.
Cones vs Rods
Cones: 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.
Rods: Most prevalent in the peripheral retina; not found in the fovea. Sensitive to low levels of light. Provide only monochromatic information. Provide poor acuity.
Neurons in the retina - photoreceptor cells
Located in the furthest back part of the retina. They express the opsin proteins that transducer light. Synapse on bipolar cells.
Neurons in the retina - bipolar cells
Relay information from photoreceptor cells to retinal ganglion cells.
Neurons in the retina - retinal ganglion cells
The only cells that send information out of the eye. Their axons form the optic nerve, which exits the retina through the optic disc (the blind spot of the retina).
Neurons in the retina - horizontal/amacrine cells
Horizontal cells and amacrine cells interconnect cells within each layer, which gives rise to complex interactions between neighbouring cells (within a layer).
Visual information pathways - visual ganglion cell action potentials
Retinal ganglion cells have action potentials, unlike most other cells in retina. Their axons go to 3 places:
1. Thalamus (specifically the lateral geniculate nucleus), which in turn projects to primary visual cortex (area V1) in the occipital lobe where visual information enters consciousness. This creates an internal (mental) representation of your entire visual space.
2. Midbrain (specifically the superior colliculi): Visual information is used here to control fast visually-guided reflexive movements. The midrabin doesn’t know what you are looking at, but it can draw attention to unexpected visual events.
3. Hypothalamus: Visual information is used here to control circadian rhythms such as sleep-wake cycles. The hypothalamus doesn’t know what you are looking at, but It knows how much light is present in your environment.
Predictive coding theory
Theory of sensory processing. The idea is that each node in the network tries to predict what its ascending inputs will look like in the next moment, based on previous experience. Top-down (descending) activity represents sensory predictions that neutralize any correctly predicted bottom-up ascending signals. Thus, what propagates up through the network may only be prediction signals, which inform the brain of how the current moment differs from what was expected. The prediction error signals that ascend through the network would cause learning to improve future precautions.
Receptive field
The receptive field of a neuron is a description of the (external) stimuli that activate it. For a neuron involved in visual processing, its receptive field is where light must be in visual space and what properties it must have to change the activity of the cell. It is in an area of visual space relative to a fixation point.
How to identify the receptive field of a cell involved in visual processing
We record the cell’s activity as the animal maintains focus on one spot on a computer screen (a fixation point). We then systematically shine light in different areas of the monitor to determine where in visual space the presence of light influences the activity of the cell. Once we find where the receptive field is, we determine if the cell responds differently to different colours or patters of light in that location.
Photoreceptor cell receptive fields
The first cell in the pathway. Photoreceptor cells release glutamate in a graded fashion dependent on their membrane potential: the more depolarized they are, the more glutamate they release. But their response to light are opposite of what you might expect. In complete darkness, photoreceptor cells sit at -40mV. This is their resting membrane potential. At rest, photoreceptor cells continuously release glutamate. When activated by light, photoreceptor cells hyper polarize to -70mV and stop releasing glutamate.
The Dark Current
Photoreceptor cells express an uncommon “leak” sodium ion channel that sits open at baseline (in the dark). The influx of sodium ions through these ion channels (the dark current) causes photoreceptor cells to sit at -40mV, where they continuously release glutamate. When an opsin protein absorbs light, it launches an intracellular g-protein signalling cascade that closes the open sodium ion channels. The closing of these ion channels causes the membrane to hyperpolarize to -70mV, at which point the photoreceptor cell stops releasing glutamate. All photoreceptor cells work like this. All the opsin proteins responsible for our conscious perception of vision are inhibitory metabotropic receptors.
Bipolar cells receptor fields
Second cell in the pathway. Bipolar cells do not have action potentials. Like photoreceptor cells, they release glutamate in a graded manner dependent on their membrane potential. There are two types of bipolar cells: OFF bipolar cells and ON bipolar cells.
OFF bipolar cells
Express normal excitatory ionotropic glutamate receptors, so their activity patterns follow that the photoreceptor cells that connect with them. In the dark, when photoreceptors are depolarized (-40mv) and releasing glutamate, OFF bipolar cells will also be depolarized and releasing glutamate. In the presence of light, when photoreceptors are hyperpolarized (-70mv) and not releasing glutamate, OFF bipolar cells will also by hyper polarized and not releasing glutamate.
ON bipolar cells
Have the opposite pattern of activity from OFF bipolar cells because they only express inhibitory (metabotropic) glutamate receptors. So, in the dark, when photoreceptor cells are releasing glutamate, ON bipolar cells will be hyperpolarized and not releasing glutamate. In the light, ON bipolar cells depolarize and release glutamate.
Retinal Ganglioon Cells (RGCs)
Are typical neurons. They have normal actions potentials and express normal excitatory ionotropic glutamate receptors.
Horizontal cells
Interconnect neighbouring photoreceptor cells. They regulate the amount of glutamate that is released from photoreceptor cells based on the activity of their neighbours. They compare the activity of neighbouring photoreceptor cells. They recognize that the centre photoreceptor cell is getting less light than its neighbours, and they accentuate this difference by counteracting the small light-induced hyperpolarization in the dimly lit cell. Thus, horizontal cells depolarize the “axon terminal” of photoreceptor cells according to how brightly lit the neighbouring photoreceptor cells are. Also release glutamate in a graded manner dependent on their membrane potential.
Bipolar cell receptive fields
The influence of horizontal cells creates a “centre-surround” organization in his receptive fields of bipolar cells.
Retinal Ganglion Cell Receptive Fields
Third cell in the pathway: Retinal ganglion cells have action potentials and a baseline firing rate in the dark. They inherit their receptive fields form bipolar cells, so they also have a “centre-surround” organization and are classified as ON or OFF cells.
ON retinal ganglion cells
Increase their rate of spiking when light is in the centre of their receptive field. They decrease their rate of spiking when light is brighter in the surround area of the receptive field.
OFF retinal ganglion cells
OFF retinal ganglion cells show the opposite pattern. They decrease their rate of spiking when light is in the centre of the receptive field and increase their rate of spiking when light is in the surround areas.
Retinal ganglion cell receptive fields in the fovea
Retinal ganglion cells in the fovea process colour information. They integrate information from many bipolar cells and have these types of receptive fields: Red on, green off. Green on, red off. Yellow on, blue off. Blue on, yellow off. (On = small circe in middle, Off = bigger surrounding circle).
Receptive fields in thalamus and V1
Retinal ganglion cells (RGCs) transmit visual information from the retina to the thalamus (the lateral geniculate nucleus). Thalamic neurons relay the information to primary visual cortex (area V1). The receptive fields of thalamic neurons are similar to that of the retinal ganglion cells. The receptive fields of neurons in V1 are the sum of many LGN neurons.
Simple cells in V1
Are sensitive to lines of light, and their receptive fields are typically organized in a center-surround fashion.
Receptive fields in primary visual cortex (V1 or striate cortex)
Neurons in V1 spike when there is a line of light in a particular orientation in their receptive field. The cell is most responsive to a vertical line of light in the centre of its receptive field. Some V1 neurons respond best to vertical lines, some to horizontal lines, and some to lines oriented somewhere in between.
Cortical columns in primary visual cortex
Every spot in your visual field is rigorously analyzed by a cortical column in V1. All neurons within a cortical column analyze the same area of visual space. Together, they analyze the orientation of light in the associated receptive field. The location of sharp transitions in the contrast/colour of light reveals borders, edges, and corners. Neurons downstream of V1 put all of this information together to identify objects and their position in space.
Visual association cortex
> 25% of the cerebral cortex is dedicated to processing visual information. All of the occipital lobe that is not primary visual cortex is considered visual association cortex. It extends to the parietal and temporal lobes, forming respectively the dorsal and ventral streams of visual info processing. Different areas of the visual association cortex are sensitive to different features of the visual environment.
Striate cortex
Part of visual association cortex. Is synonymous with primary visual cortex (Area V1).
Extrastriate cortex
Part of visual association cortex. Is synonymous with visual association cortex (areas V2, V3, V4, etc.)
Dorsal stream
The dorsal stream of visual information starts in primary visual cortex and ends in posterior parietal lobe. It is involved in identifying spatial location. It encodes where objects are, of they are moving, and how you should move to interact with them or avoid them.
The ventral stream
Starts in primary visual cortex and ends in inferior temporal lobe. It is involved in identifying form (shape). It encodes what the object is and its colour.
Monocular vision
Some V1 neurons respond to visual input from just one eye.
Binocular vision
Most V1 neurons respond to visual input from both eyes.
Depth perception
There are many monocular cues that can be used to estimate depth, such as relative size, amount of detail, relative movement as we move our eyes, etc. These are the cues we use to appreciate depth when looking at a photograph or TV screen (any flat, 2-dimensional image). Only the eye is required to perceive depth with monocular cues.
Stereopsis
The perception of depth that emerges from the fusion of two slightly different projections of an image on the two retinas. The difference between the images from the two eyes is called retinal disparity. It results from the horizontal separation of the two eyes. It improves the precision of depth perception, especially for moving objects. Two eyes are helpful when playing sports, but also (to some extent) when pouring a glass of water.
Agnosia
A deficit in the ability to recognize or comprehend certain sensory information, like specific features of objects, people, sounds, shapes, or smells, although the specific sense is not defective nor is there any significant memory loss. Relates to a problem in some sensory association cortex, not to problems that relate to the sensory neurons themselves or to the primary sensory areas.
Akinetopsia
A deficit in the ability to perceive movement - is a type of visual agnosia caused by damage to the dorsal visual stream in the parietal lobe of the cerebral cortex.
Cerebral achromatopsia
In contrast to regular chromatopsia, it is a visual agnosia caused by damage to the cerebral cortex in the ventral visual stream. People deny have any perception of colour. They say everything looks dull or drab, and that it is all just “shades of grey”. (People born with regular achromatopsia don’t say those things, because they have no conception of colour).
Prosopagnosia
Failure to recognize particular people by sight of their faces; a visual agnosia caused by damage to the fusiform gyrus (fusiform face area) in the ventral visual stream.
Sound waves
When an object vibrates, it causes molecules in the surrounding air to alternately condense and rarefy (pull apart). These fluctuations in air pressure give rise to a sound wave that travels away from the object at approximately 700 miles per hour.
Audition (hearing)
The human ear can transducer fluctuations in air pressure when the length of the sound wave is between 0.017 and 17 meters long. These sound waves are generated when physical objects vibrate between 20 and 20,000 times per second.
Three physical dimensions of sound
- Loudness
- Pitch (tone)
- Timbre
Loudness
Corresponds to the amplitude or intensity of the molecular vibrations, the relative difference in the density of air molecules between compressed and rarified air. This dimensions determines how far the sound wave will travel.
Pitch (tone)
Corresponds to the frequency of the molecular vibrations (or the distance between neighbouring peaks of compressed air). It is measured in hertz (Hz, cycles per second). Every frequency has a corresponding wavelength.
Timbre
Corresponds to the complexity of the sound wave. Our brains learn to recognize the timbre of sound waves to identify the source of the sound (e.g., which instruments is playing the note middle C).
Pinna
Sound is funnelled through the pinna (outer ear).
Tympanic membrane
At the end of the ear canal (still outer ear), sounds cause the tympanic membrane (the eardrum) to vibrate. These vibrations are transferred to the middle ear.
Ossicles
The middle ear is comprised of three ossicles (small bones): the malleus, incus and stapes.
Oval window
Vibrations of the tympanic membrane cause the ossicles to vibrate, which in turn cause the membrane behind the oval window to vibrate.
Cochlea
Vibrations of the oval window are transmitted to the fluid-filled cochlea (the inner ear), which is a long coiled tube-like structure that contains sensory neurons.
Basilar Membrane
High pitched notes are detected where the basilar membrane is thick and narrow (closest to the oval window). Low notes are detected where the basilar membrane is thin and wide. The basilar membrane is kind of like a xylophone backwards, where the longest wood bars correspond to the low notes.
The cochlea is divided into three longtudinal divisions
Scala vestibuli, scala media, and scala tympani.
Organ of Corti
The receptive organ. It consists of the basilar membrane on the bottom, the tectorial membrane on the top, and auditory hair cells in the middle.
Hair cells and Cilia
The cells that transduce sound are called hair cells because of their physical appearance. Their hair-like extensions are called cilia. Outer hair cells have cilia that are physically attached to the rigid tectorial membrane. The cilia of inner hair cells are not attached to anything. They sway back and forth with the movement of the solution. Sound waves cause the basilar membrane to move relative to the bacterial membrane, which causes hair cell cilia to stretch and bend. The movement of the cilia pulls open ion channels, which changes the membrane potential of hair cells.
Inner & Outer Hair Cells
Although there are 3 times more outer hair cells than inner hair cells, only inner hair cells transmit auditory information to the brain. Outer hair cells act like muscles to adjust the sensitivity of the tectorial membrane to vibrations. By regulating the flexibility of the tectorial membrane, outer hair cells influence the sensitivity of inner hair cells to specific frequencies of sound (i.e., different notes). People who do not have working inner hair cells are completely deaf. People who do not have functional outer hair cells can hear, but not very well.
Tip links
The cilia of hair cells are connected to each other by tip links - elastic filaments that attach the tip of one cilium to the side of adjacent cilium.
Insertional plaque
The point of attachment of a top link to cilium is called an insertional plaque. Each insertional plaque has a single ion channel in it that opens and closes according to the amount of stretch exerted by the tip link.
Loud Noise and tip link breakage
Lord noises can easily break the tip links that interconnect each cilia. And hair cells cannot transmit auditory information without tip links. Fortunately, tip links usually grow back within a few hours. Tip link breakage generally corresponds to temporary hearing loss. Tip link breakage is probably a protective measure, because too much glutamate release onto the cochlear nerve causes permanent cell death.
Place coding
Because of how the cochlea and basilar membrane are constructed, acoustic stimuli of different frequencies cause different amounts of movement along the basilar membrane. Higher frequency sounds cause bending of the basilar membrane closest to the stapes, resulting in more hair cell activity in that area. Moderate to high frequencies are entirely encoded by place coding. Human speech is in this frequency range.
Rate coding
Low frequency sounds are processed using a rate coding system: the pattern of neurotransmitter release from the hair cells deepest in the cochlea (furthest from the stapes) determine the perception of low frequency sounds.
Graph of three curves indicating sensitivity of inner hair cells
Low points of three solid curves indicate that these inner hair cells will respond to faint sound only if it is of a specific frequency. If the sound is louder, cells will respond to frequencies above and below their preferred frequencies. Lesions targeted to outer hair cells disrupt the responsiveness of inner hair cells to specific sounds.
Pitch perception
Moderate to high frequencies are encoded by place coding. Low frequencies are partly encoded by rate coding.
Loudness
Loudness corresponds to the total number of hair cells that are active and their overall activity levels.
Timbre
Timbre is perceived by assessing the precise mixture of hair cells that area active throughout the entire cochlea.
Fundamental frequency
The lowest and most intense frequency of a complex sound. This frequency is most often perceived as sound’s basic pitch.
Overtone
Sound wave frequencies that occurs at integer multiples of the fundamental frequency.
Timbre
The specific mixture of frequencies (fundamental frequency plus overtones) that different instruments emit when the same note is played. It is the complexity of the sound wave. We analyze the timbre of a sound and how the timbre changes over time to identify which instrument made the sound.
Cohlear implants
Cochlear implants for the hearing-impaired take advantage of the place coding system of the cochlea. They elicit the perception of different notes by stimulating different places along the cochlea (with 20 to 24 evenly spaced electrodes). Loudness is controlled by the frequency stimulation.
Interaural cues
Differences in sound perception between the two ears. One of the main ways we localize sounds is by analyzing the timing difference between the 2 ears (which ear heard the sound first).
Interaural loudness
For high frequency sounds (above 800Hz) we use intramural loudness differences to help identify the location of a sound (which ear heard it louder). This approach is possible because the loudness of a high-pitched (high-frequency) sound is significantly dampened by the head.
Localizing low frequency sounds
To help localize low frequency sounds (below 800 Hz, which corresponds to wavelengths that are longer than the width of the head), the brain analyzes the phase differences between the two ears.
Identifying the height of a sound
To discriminate whether a sound is coming in front, behind, or above you, we analyze the timbre of the sound wave. The shape of our outer ear (pinna and ear canal) creates a direction-selective filter; different frequencies are enhanced/attenuated when sound enters our ears from different directions. These effects are highly individual (depending on the shape and size of the outer ear). We are not born with this skill - must continuously learn.
From the Ear to Primary Auditory Cortex
- The organ of Corti sends auditory information to the brain via the cochlear nerve.
- These axons synapse in the cochlear nuclei of the medulla, where copies of the signal are made to be analyzed in parallel ascending paths.
- 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.
- Axons from the inferior colliculi synapse in the medial geniculate nucleus of the thalamus, which in turn relays the information to the…
- Primary auditory cortex in the temporal lobe
Tonotopic representation
Like the Basilian membrane, the primary auditory cortex respond best to different frequencies. In this organization different frequencies of sound are analyzed in different places of auditory cortex.
Primary auditory cortex (core region)
In the upper section of the temporal lobe, mostly hidden in the lateral fissure.
Auditory association cortex
The belt and parable regions refer to the auditory association cortex. Like visual information, auditory information is analyzed in “where” and “what” streams.
The posterior (dorsal) auditory pathway
Involved in sound localization. This pathway meets up with the “where” vision pathway in the parietal lobe.
Anterior auditory pathway
Important for recognizing what produced a sound (not the location of the sound). It is sometimes called the auditory object recognition pathway, and it extends from the temporal lobe into the frontal lobe.
Auditory Agnosia
Music and language are special, complex forms of auditory processing, and brain damage in auditory association cortex can cause very specific types of auditory agnosia. Different areas of auditory association cortex process the melody, rhythm, and harmony (overtones) of music. Other areas of auditory association cortex process the melody, rhythm, and harmony (overtones) of music. Other areas of auditory association cortex are involved in the perception of sound as pleasant (consonant) or unpleasant (dissonant), and certain combinations of musical notes can trigger emotions. There are many types of auditory agnosias.
Amusia
Amusia is the inability to perceive or produce melodic music. People with amuse might be unable to sing or recognize the happy birthday song. People with amusia can often converse and understand speech. They can also recognize environmental sounds. They can even recognize the emotions conveyed in music, but they will typically be unable to tell the difference between consonant music (pleasant sounding) and dissonant music (unstable) even though these sounds might alter their emotional state just as they do in other people.
Vestibular System
The inner ear beyond the cochlea. Vestibular system detects gravity and tilts and turns of the head. Cochlea detects sound. Vestibular system doesn’t always produce readily definable, conscious sensations. But it contributes to our sense of balance, maintains an upright head position, and corrects eye movements to compensate for head movements. Disruptions in the vestibular system can cause dizziness and nausea.
Otolith organs (vestibular sacs)
Two distinct structures: the utricle & saccule - that monitor the angle of the head and linear acceleration of the head.
Semicircular canals
Three ring-like, fluid-filled structures that detect changes in head rotation (angular acceleration). In each semicircular canal is one bulge called the ampulla, where a gelatinous mass (cupula) pulls open hair cells in response to movement of fluid in the canals.
Otolith Organs
In the otolith organs (the utricle & saccule), it is the weight of a stone of calcium carbonate (an otolith) that pulls open hair cell ion channels to indicate the angle of the head and whether it is accelerating along a linear path. One otolith sits in the horizontal plane, and the other sits in the vertical plane.
Somatosensory System
Provides information about touch, pressure, temperature, and pain, both on the surface of the skin and inside the body.
Three interacting somatosensory systems
- Exteroceptive system (cutaneous/skin senses): responds to external stimuli applied to the skin (e.g., touch and temperature).
- The interoceptive system (organic senses): provides information about conditions within the body and is responsible for efficient regulation of its internal milieu (e.g., heart rate, breathing, hunger, bladder).
- The proprioceptive (kinesthesia) system: monitors information about the position of the body, posture, and movement (e.g., the tension of the muscles inside the body).
The Cutaneous Senses
The cutaneous senses (skin) encode different types of external stimuli:
1. Pressure (touch) is caused by mechanical deformation of the skin
2. Vibrations occur when we move our fingers across a rough surface
3. Temperature is produced by objects that heat or cool the skin
4. Pain can be caused by many different types of stimuli, but primarily tissue damage.
Epidermis
Outer most layer of the skin. (“above dermis”). Cells here get oxygen from the air (not the blood).
Dermis
Middle layer of the skin.
Hypodermis or Subcutaneous
The deepest layer of the skin. (“below the skin”). Sensory neurons are scattered throughout these layers.
Merkel’s disks
Respond to local skin indentations (simple touch).
Ruffini Corpuscles
Are sensitive to stretch and the kinaesthetic sense of finger position and movement.
Pacinian corpuscles
Respond to skin vibrations
Glabrous skin
Hairless skin. E.g., palms of hands and feet.
Free nerve endings
Primarily respond to temperature and pain
Meissner’s corpuscles
Only found in glabrous skin. They detect very light touch and localized edge contours (brail-like stimuli).
Temperature / two categories of thermal receptors
Two categories of thermal receptors: those that respond to warmth and those that respond to coolness. Pain information is also conveyed by some of these cells. This information is poorly localized, and the axons that carry it to the CNS are unmyelinated or thinly myelinated. Some of the receptor proteins that are sensitive to temperature can also be activated by certain ligands.
Pain
Sensations of pain and temperature are transducer by free nerve endings in the skin. There are several types of pain receptor cells (usually referred to as nociceptors - “detectors of noxious stimuli”).
High-threshold mechanoreceptors
A type of pain receptor. Pressure receptor cells. They are free nerve endings that respond to intense pressure, like striking, stretching, or pinching. Other types of free nerve endings respond to extreme heat.
2 main pathways in which axons from skin, muscles, and internal organs enter the CNS via spinal nerves
- Poorly localized information (e.g., crude touch, temperature, and pain) crosses over the midline in the spinal cord, just after the first synaptic connection. This information ascends to the thalamus through the spinothalamic tract.
- Highly localized information (e.g., fine touch) ascends ipsilaterally through the dorsal column of the spinal cord. The first synapse in this pathway is in the medulla. From there the information crosses over to the contralateral side as it ascends to the thalamus.
Both pathways get bundles together in the midbrain before synapsing in the thalamus. from there, information goes to primary somatosensory cortex in the parietal lobe.
The Somatosensory Homunculus
When different sites of primary somatosensory cortex are electrically stimulated, patients report somatosensory sensations in specific parts of their bodies. The relationship between cortical stimulations and body sensations is reflected in a somatotropin map of the body surface. The somatotopic map is often referred to as the somatosensory homunculus (“little man”).
Tactile Agnosia
Patients with tactile agnosia have trouble identifying objects by touch alone. When touching an object, people might think this is that: pine cone –> brush, ribbon –> rubber band, snail shell –> bottle cap. However, these patients can often draw objects that they are touching, without looking, and they can sometimes identify objects from their drawings.
Phantom Limb
Phantom limb is a form of pain sensation that occurs after a limb as been amputated. Amputees report that the missing limb still exists and that it often hurts. One idea is that a phantom lib is due to confusion in the somatosensory cortices. The brain gets nonsense signals and it has difficulty interpreting them.
Six different categories of taste receptors:
- Sweetness (molecules of sugar): detected with a single metabotropic receptor.
- Umami (molecules of glutamate/glutamine): detected with a single metabotropic receptor
- Bitterness (a variety of molecules): detected with 50 different metabotropic receptors that bind different bitter molecules)
- Saltiness (positive ions such as sodium): detected with an ion channel that is highly permeable to sodium.
- Sourness (pH level; the concentration of free hydrogen ions): detected with an ion channel that is highly permeable to free protons.
- fat (fatty acids): detected with metabotropic receptors and fatty acid transporters.
Perception of gustatory information
Transduction is similar to chemical transmission that takes place at synapses. When a tasted molecule binds to a taste receptor protein, it produces a change in membrane potential (either directly trough an ion channel or through G protein signalling cascades). Different tastes relate to the activation of different types of taste receptor proteins.
Taste buds and taste receptor cells
Taste buds contain 20 to 150 taste receptors cells, some for each type of taste (sugar, Unami, bitter, salt, sour, or fat). Taste receptor cells do not have traditional action potentials. They release neurotransmitter in a graded fashion. Taste receptor cells are replaced about every ten days, because they are directly exposed to a rather hostile environment.
Studying the taste system but manipulating the DNA of mice
To identify the sugar taste receptor, researchers remove specific genes from their genome and then test if mice can discriminate between regular water and sugar water. These studies demonstrate that much of taste processing is innate (hard-wired from birth to be either pleasurable or aversive).
Rewarding/aversive taste receptor cells
Sugar and Unami taste receptor cells are instinctively rewarding/reinforcing. Direct stimulation to them (or their downstream structures in the cerebral cortex) is inherently reinforcing. Bitter taste receptor cells are instinctively aversive.
Odorant molecules
The olfactory system is specialized for identifying specific molecules called odorants. They are volatile substances that have a molecular weight in range of approximately 15 to 300. Most of them are lipid soluble and of organic origin, however many substances that meet these criteria have no door.
Receptor proteins that transduce odorants into a change in membrane potential
are metabotropic G protein-coupled receptors. Humans express around 400 different types of odorant receptors. Each one is sensitive to a specific molecule.
Olfactory epithelium
The tissue of the nasal sinus that sits underneath the skull (the cribriform plate) and contains olfactory receptor cells. Each olfactory cell expresses only one type of olfactory receptor protein.
Glomeruli
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). Thus, each glomerulus processes a distinct odour.
innately good or bad odors
Unlike taste, doors are largely not hard wired to be innately good or bad. Whether we like or dislike an oder is related to learned associations.
How does olfactory information get relayed
Does not get relayed in the thalamus. It goes directly to primary olfactory cortex in the temporal lobe and the amygdala.
Pheromones
Although most doors are not innately perceived as good or bad in young animals, pheromones are different. Pheromones are molecules released by one animal to signal something to another member of the same species. Behavioural responses to pheromones are largely innate (hard-wired from birth). Pheromones strongly influence the behaviour of many organisms, but existence in humans is controversial.
In many animals, especially insects, pheromones are used to
Attract or repel other members of the same species, signal attractiveness and sexual receptivity, mark a path to follow (as seen in ants), signal danger.
Pheromone Signaling - vomeronasal organ
In mammals, the initial transduction and processing of pheromones occurs in the vomeronasal organ and ‘accessory olfactory bulb’, which are next to but distinct from the regular olfactory epithelium and ‘main olfactory bulb’, which process regular odors.
Pheromone Signaling - Vomeronasal receptors
Pheromones are detected by metabotropic vomeronasal receptors. These receptors are only distantly related to the olfactory receptors that detect normal doors, highlighting their different role. Human, apes, and birds to not have functional vomeronasal organs. They only have regular olfactory epithelium that detects normal odors.
Rodent Pheromone Effects
Many mammals release pheromones in their urine. These molecules are usually not airborne. They must be actively sniffed or tasted to be detected. Rodents sniff each other’s genitals and each others’ urine, and pheromone detection strongly influences their sexual behaviour. Female to male pheromone signaling is especially powerful. Male to female pheromone effects are more subtle.
Lee-Boot Effect
When female mice are housed together (without any male urine present), their estrous cycles slow down and eventually stop.
Whitten Effect
Pheromones in the urine of male mice can trigger synchronous estrus cycles in groups of female mice.
Vandenbergh Effect
Earlier onset of puberty seen in female animals that are housed with males.
Bruce Effect
The tendency for female rodents to terminate their pregnancies following exposure to the scent of an unfamiliar male.
Homeostasis
Cells require a viable temperature and food and water for survival. The temperature cannot be too hot or cold. Food and water availability must be above some threshold. Homeostasis refers to the process of actively maintaining internal condition, particularly with respect to food and water availability and body temperature. Animals live in diverse environments because they can maintain homeostasis.
Unconscious temperature regulation
When the temperature of warm-blooded (endotherm) animals deviates from a set point (-37c), the body launches corrective mechanisms. Cold-blooded (ectotherm) animals are not very good at maintaining their body temperature, so their ability to move and function is highly dependent on the ambient temperature.
Unconscious temperature regulation when the body is too cold
Basal metabolic rate increases; calories are burned to generate heat. The body shivers, a way of burning calories to generate heat. Peripheral blood vessels constrict, moving blood to interior of the body so less heat is lost through the skin.
Unconscious temperature regulation when body is too hot
Animals sweat or pant like a dog (breathe heavily); water evaporation has a cooling effect. Peripheral blood vessels expand; blood moves closer to the skin so body. heat can dissipate into the surrounding air.
Conscious temperature regulation
When our body temperature becomes uncomfortable, we consciously experience a need state. Need states are motivating. They drive us, push us to correct the specific problem. When a need becomes satisfied, we typically experience relief or pleasure. The anticipation of pleasure can motivate us (pull us) to perform an action, even in the absence of a corresponding need.
Regulation of thirst and fluid intake
We primarily lose water by urinating, sweating, and breathing. We consciously experience thirst when there is either:
1) not enough water inside cells (osmometric thirst) or 2) not enough blood (liquid) in our circulatory system (volumetric thirst)
Tonicity (Osmometric thirst)
Tonicity refers to the relative concentration of dissolved molecules (solutes in solution) on either side of a membrane that is permeable only to the solution, not to the solutes dissolved in it. Diffusion is the process by which molecules move from areas of high concentration to areas of low concentration. Osmosis refers to the movement of a solution (solvent) from areas of high concentration (low tonicity) to areas of low concentration (high tonicity). Thus, tonicity describes the direction solvent will flow across a membrane that is only permeable to the solvent.
Isotonic solution
Similar concentrations of solute on either side of the membrane. The cell will neither gain nor lose water.
Hypotonic solution
Solute is less concentrated outside the cell than in, so water will enter the cell
Hypertonic solution
Solute is more concentrated outside the cell than in, so water will leave the cell
Body Fluid Compartments
Water freely moves in and out of cells, going wherever the tonicity (the concentration of dissolved solutes) is higher. Cells take in salts and other solutes as needed from extracellular fluid. Across time, intracellular solute concentrations are fairly stable, while extracellular solute concentrations vary according to what we weather and drink.
Tonicity when we drink water
When we drink water, it lowers the tonicity of extracellular fluid, causing cells to expand in size as water moves into them from the extracellular fluid. Excess water is quickly eliminated by urine production.
Tonicity when we consume salt
When we consume salt, it increases the tonicity of extracellular fluid, causing cells to shrink in size as water moves out of them. This physical contraction of cells triggers osmometric thirst.
Osmometric thirst
Hypertonic (salty) solutions cause cellular dehydration (cells lose water and shrink in size). Osmoreceptors are neurons whose membrane potential is sensitive to the size of the cell. The release of neurotransmitter from osmoreceptors relates to the volume of these cells.
Volumetric thirst
Occurs when there is not enough blood circulating in the body. The. heart needs a certain amount of blood to keep beating. People feel an intense thirst after they lose a lot of blood because of volumetric thirst. Low blood pressure causes cells in the kidneys to release an enzyme called renin, which initiates a cascade of chemical reactions in the blood.
Thirst
Feelings of thirst relate to neural activity in a few different brain regions, particularly a hypothalamic area known as anteroventral tip of the third ventricle (the AV3V region). In human fMRI studies, feelings of thirst activate neurons in the AV3V region as well as anterior cingulate cortex.
The act of drinking when thirsty
Drinking immediately quenches feelings of thirst, and some thirst related neural activity immediately dissipates upon drinking (before water reaches the relevant cells), but AV3V neurons generally remain active until the water reaches them (long after people have stopped drinking).
Food mostly consists of
Sugars (carbohydrates), Lipids (triglycerides), Amino acids (proteins).
Blood Glucose
The pancreas monitors blood glucose levels: When blood glucose is high, the pancreas releases insulin. When blood glucose in low, the pancreas releases glucagon. Insulin causes blood glucose to be stored as glycogen (in liver and muscle cells). Glucagon causes glycogen to be broken down into glucose.
Glycogen
Sometimes referred to as animal starch. Represents our short-term storage of glucose. We build up glycogen levels when we eat (when insulin is released). We deplete glycogen levels between meals. Glycogen can store up to 2000 calories.
Insulin
Pancreatic hormone that facilitates: 1) conversion of glucose into glycogen 2) entry of glucose and amino acids into cells of the body, and 3) transport of fats into adipose tissue.
Glucagon
Pancreatic hormone that promotes 1) conversion of liver glycogen into glucose, and 2) conversion of adipose triglycerides into fatty acids.
Cells absorption of glucose
Cells in the brain can always take in glucose (using a glucose transporter). Most cells outside the brain use a glucose transporter that requires insulin to be functional, which means they can only take in glucose when insulin is present (when blood glucose levels are high). In the absence of insulin (about 2 hours after a meal), cells in the body cannot take in glucose. They can only ketones (made from fatty acids) for energy.
Blood Lipids
Insulin causes fatty acids to be stored as triglycerides in adipose tissue (fat cells). Triglycerides represent our long-term storage of energy. Glucagon causes triglycerides to be broken down into fatty acids. 1 triglyceride = 1 glycerol molecules + 3 fatty acids: the liver converts glycerol into sugar and fatty acids into ketones.
Cells in the presence of insulin
In the presence of insulin, all cells can use glucose for energy. Glucose is also stored for later use.
Glycogen in the presence of glucagon
In the presence of glucagon, glycogen is broken down into glucose for cells in the brain, while cells in the body switch to using ketones (from fatty acids) for energy.
Energy Homeostasis System
Cells in the liver monitor glucose levels, and this information is brought to the brain by the 10th cranial nerve (the vagus). One controller of hunger is blood glucose levels. The stomach releases different signalling molecules when empty and when full. Some of these signalling molecules reach the brain and influence hunger.
Signals from the Stomach
An empty stomach is communicated to the brain by the stomach’s release of a peptide called gherkin. Levels of circulating ghrelin increase when hunger and fall with satiation. Exogenous administration of ghrelin increases hunger and food intake. Swelling of the stomach can slightly reduce hunger, but it mostly just causes a bloated feeling.
Hormones CCK and GLP-1
Regulate the release of digestive enzymes and insulin. They are released by the intestines in proportion to the number of calories ingested, and their entry into the brain elicits feelings of satiety.
CCK and GLP-1 for weight loss
Repeated administration of CCK to healthy people does not reliably cause sustained weight loss. It sometimes decreases meal size, but people typically respond by eating small meals more frequently. In contrast, GLP-1 agonists have recently proven to be highly effective in reducing hunger and weight in most people. These drugs were initially developed to boost insulin signalling in diabetics.
Long-term fat storage
Beyond monitoring blood glucose and food in the stomach, the body also monitors fat levels. The body wants to ensure there is enough fat to make it between meals. In many cases, when a healthy animal is force-fed so that it becomes heavier than normal, it will reduce its food intake once it regains control over how much it eats.
Signals that come from fat cells - Leptin
Leptin is a circulating hormone that is secreted by adipocytes (fat cells). Leptin levels correlate with the amount of fat in the body. As fat cells grow and proliferate, leptin levels increase. If leptin levels fall below some threshold, animals feel intense hunger. To some extent, leptin levels regulate the sensitivity of hypothalamic neurons to short-term satiety signals. Exogenous administration of leptin can slightly decrease meal size in healthy people, but this effect is short-lived. However, exogenous leptin administration is a lifesaver for people who are unable to produce leptin due to a genetic mutation.
Congenital leptin deficiency
Ob mouse - Strain of mice whose obesity and low metabolic rate are caused by mutation that prevents production of leptin
Emergency hunger circuits
Emergency hunger circuits are activated when a specific critical need to ear or not eat overrides energy homeostasis circuitry.
Glucoprivation (hypoglycemia)
Dangerously low blood-glucose levels (i.e., not enough immediately available sugar in the blood) can cause intense hunger. Glucoprivation can result from excessive insulin signalling and from drugs that inhibit glucose metabolism.
Lipoprivation
Dangerously low levels of fat (i.e., not enough fat on the body or free fatty acids in the blood). Can be caused by drugs that inhibit fatty acid metabolism.
Emergency Hunger
When the brain senses that energy stores are dangerously low (glucoprivation or lipoprivation), it launches an emergency cascade of effects:
1. Insulin release is suppressed, and glucagon release is triggered.
2. Short-term satiety signals are ignored.
3. Energy expenditure slows (basal metabolic rate), halting growth and reproductive systems.
4. A potent and sustained feeling of hunger takes hold.
Diabetes
A condition where people are either insensitive to insulin signalling or they do not release enough insulin. Diabetes results in high blood glucose levels and an inability to store glucose as fat. If left untreated, it leads to intense thirst and progressive weight loss (especially for type 1, in which insulin is not being released). As fat cells become depleted, leptin levels fall, and a lipoprivation-related feeding emergency takes hold, resulting in intense hunger, even if there is tons of glucose in the blood.
Hypothalamus and hunger
A key regulator of hunger. Two cell populations in the arcuate nucleus of the hypothalamus have opposing influences on hunger. Stimulation of one cell population - the neurons that co-release the peptides AGRP and NPY - causes dramatic overeating. Leptin and other satiety signals inhibit these neurons.
Arcuate Nucleus of the Hypothalamus
AGRP/NPY neurons promote hunger. They are inhibited by leptin and activated by gherkin. Neighbouring (POMC) neurons inhibit hunger. They are activated by leptin and inhibited by ghrelin. Feelings of hunger partially relate the balance of activity between these two cell populations. These two cell populations project other the paraventricular nucleus (PVN) of the hypothalamus. Some neurons in this area stop firing when the body has dangerously low levels of fat (leptin).
Paraventricular Nucleus (PVN) of the Hypothalamus
Artificially increasing PVN nueron activity does not substantially/reliably change hunger, but the inhibition of some cells in this area can generate intense hunger. These cells seem to trigger a lipoprivation response.
Trader-Willi Syndrome
Prader-Willi syndrome is a rare chromosomal abnormality in which up to 7 genes are deleted from chromosome 15. One of these genes is critical for the development/survival of a population of PVN neurons. People with this syndrome are born with very low muscle mass and have little interest in eating. But between 2 and 8 years of age, they develop a heightened, permanent and painful sensation of hunger, a feeling of starving to death. Average life expectancy in. the US is 30; most die of obesity-related causes. People with his 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.
The Modern Obesity Epidemic
About 50% of the variability in people’s body fat is due to genetic differences. Natural variations in metabolic efficiency are one of the most important factors. Some people’s genes are not well-suited for our current food environment. There is a hedonic aspect to hunger. Food can be delicious and reinforcing even when people are not hungry. But this is truer for some people than others. Neuroscientists are using hormones released by the gut to(such as GLP-1) as tools to study neural control of hunger.
Bariatric Surgery
Modifies the stomach, small intestine, or both. The most effective form is called the Roux-en-Y gastric bypass (RYGB). Limits the amount of food that can be eaten during a meal. The second part of small intestine (the jejunum) is cut and attached to the top of the stomach. The stomach is also stapled to make it much smaller.
Sexual Dimorphism
Condition where the two sexes of the same species exhibit different characteristics beyond the differences in their sexual organs. May be subtle or exaggerated and can include different size, weight, colour, behaviour and cognition. They include secondary sex characteristics (i.e., features that occur during puberty).
Sexual dimorphic behaviours
Behaviours that take different forms, or occur with different probabilities, or under different circumstances across males and females of the same species.
Sexual dimorphic behaviours in mammals
The most striking category of sexual dimorphic behaviours in mammals are reproductive behaviours, including courting, mating, parenting, and most forms of aggression.
Sexual dimorphic behaviours in humans
There are differences between the sexes, on average, in their mixture of talents, temperaments, and interests. The brain gives rise to sexual dimorphic behaviours because it is a sexual dimorphic organ. The average size and interconnectivity of different brain regions vary according to sex. Sex differences in the brain can be the result of biology, socialization, and the interaction of the two.
Socialization children
When socializing children, we sometimes support whatever behaviours spontaneously emerge. More commonly, we pre-emptively encourage/discourage certain behaviours to ensure their expression is congruent with our values and the dominant culture.
How does the study of biology help resolve arguments of socialization
Things that are innate, natural, or biological are not inherently good or bad. The value of these things is determined by people based on their culture.
Sex and reproductive behaviour
The developmental program of many species produces male and female specializations. In these species, reproduction involves sex and the fusion of specialized cells known as gametes (one from each parent).
Gametes
Mature reproductive cells made by gonads (ovaries or testes). They are either ova (egg cells) or sperm. Unlike all other cell sin your body, which typically have 23 pairs of chromosomes (23 from your biological mother and 23 from your biological father), gametes only have one copy of each chromosome (a mix from mother and father). One pair of chromosomes are called the sex chromosomes, as they usually determine the organism’s sex. They come in X and Y varieties.
Five factors present at birth are typically used to determine an animal’s biological sex
- Sex chromosomes: XX and YY
- Gonads: testes or ovaries
- Sex hormones: androgen signalling
- Internal reproductive anatomy
- External anatomy
Generally, the five factors are either all male or all female. Atypical combinations give rise to intersex conditions, in which the person cannot be distinctly identified as male or female.
Embryonic Sex Organs
All embryos contain precursors for both female and male sex organs. Undifferentiated gonads, Mullerian system, Wolffian system.
Undifferentiated gonads
Embryonic precursor of ovaries/testes. During the second month of gestation, the undifferentiated gonads typically develop into ovaries or testes.
Mullerian system / Wolffian system
Mullerian system: Embryonic precursors of female internal sex organs.
Wolffian system: Embryonic precursors of male internal sex organs.
During third month of gestation, typically either the Mullerian or Wolffian system develops while the other withers away.
Male Sex Organ Development
The SRY gene that is normally located on the Y chromosome encodes a protein that causes undifferentiated fetal gonads to develop into testes. This gene overpowers XX-ovary instructions, so XXY individuals develop testes. Embryonic testicular release of: 1) Anti-Mullerian hormone: stops development of Mullerian system 2) Androgens (testosterone): triggers development of male sex organs - internal and external.
Defeminizing effect
Effect of anti-Mullerian hormone early in development, which prevents development of the female-typical internal anatomy.
Masculinizing effect
Effect of androgen hormones early in development, which triggers development of male-typical anatomy.
Androgens
Male sex hormones.
Testosterone
Testosterone is the principal mammalian androgen. It is released by the testes, and it triggers development of the Wolffian system (internal male sex anatomy). Some testosterone is converted into dihydrotestosterone, which is what triggers development of external male sex anatomy.
Female Sex Organ Development
XX chromosome –> Development of ovaries –> Which are largely silent until puberty –> Puberty is triggered by hormones released from gonads (ovaries or testes).
The ovaries do not release any critical signalling molecules before puberty. So, what triggers development of female reproductive anatomy?
In the absence of anti-Mullerian signalling, the Mullerian system develops into internal female reproductive anatomy, which includes inner vagina, uterus, and fallopian tubes. In the absence of testosterone signalling external female sex organs (vulva) develop while the Wolffian (male internal) system withers away.
Turner Syndrome / Swyer Syndrome
Turner Syndrome: When you only have one sex chromosome (X-). Associated with other developmental abnormalities on account of missing a full chromosome.
Swyer Syndrome: When you are XY but have a bad SRY gene.
In both cases, gonads do not develop (neither testes nor ovaries), but female-typical sex organs develop normally. People without gonads are infertile. They. also do not naturally experience puberty.
Insufficient anti-Mullerian hormone signalling
Will cause insufficient anatomical defeminization: both male and female internal sex organs will develop and get tangled together. There is often functional external male genitalia.
Androgen insensitivity syndrome
Results in anatomical defeminization with partial or no masculinization. In severe cases, no internal sex organs develop. In these cases, people typically develop normal external female genitalia and identify as heterosexual women, but they will be infertile and have a short vagina. In mild cases, the external genitalia is fully masculinized. Intermediate cases are associated with ambiguous external genitalia.
Organizational Effects of Sex Hormones
Sex hormones influence the development of the body and brain. These effects are permanent and put you on a particular trajectory going forward. Behavioural defminization, behavioural masculinization.
Behavioural defeminization
Refers to organizational effect of androgens on the brain that prevent animals from displaying female-typical behaviours in adulthood.
Behavioural masculinization
Refers to organizational effect of androgens on the brain that enables animals to engage in male-typical behaviours in adulthood.
Activational Effects
Puberty causes sex hormones to be released by the gonads, which influence both body and mind. The production of sperm, ovulation, and general horniness are all examples of activation effects. How the mind and body respond to activational hormone signalling in adulthood depends on how the body and brain were organized by hormone signalling in utero.
Sexual Maturation
Puberty is initiated when the hypothalamus secretes gonadotropin-releasing hormones (GnRH), which stimulate the release of gonadotropic hormones by the anterior pituitary gland.
Kisspeptin
Neuropeptide produced by neurons in the hypothalamus that initiates puberty and maintains reproductive ability. by triggering release of gonadotropin-releasing hormone.
Gonadotropin-releasing hormone
Hypothalamic hormone that stimulates anterior pituitary g land to secrete gonadotropic hormones.
Gonadotropic hormones
Hormones of pituitary gland (follicle-stimulating hormone, FSH, and luteinizing hormone, LH) that have stimulating effect on cells of gonads.
Male Sexual Behaviour
Human males are like other male mammals in their behavioural responsiveness to testosterone. With normal levels of testosterone, males can be fertile; without testosterone, sperm production ceases, and sooner or later, so does the ability to have sex.
A castrated male rat
A castrated male rat will cease sexual activity, but it can be reinstated with an injection of testosterone.
Men taking a gonadotropin-releasing hormone antagonist
Will not show testicular release of androgens and have a decrease in sexual interest and intercourse.
Estrogen
Class of sex hormones release by the ovaries that cause maturation of the physical features and characteristic of females, such as as growth of breast tissue and female genitalia.
Estradiol
Principal estrogen of many mammals, including humans.
Hormonal control of female reproductive cycles
Both menstrual and estrous cycles are controlled by the two ovarian hormones estradiol and progesterone
Menstrual cycle
Female reproductive cycle of most primates, including humans. Characterized by menstruation (if pregnancy does not occur), concealed ovulation, and the absence of a mating season. Sexual arousal is somewhat influenced by ovarian hormones, but ability to mate is not. Animals with a menstrual cycle exhibit sexual activity throughout the cycle.
Estrous Cycle
Female reproductive cycle of most mammals (other than most primates). Females that have estrous cycles do not menstruate; they reabsorb their endometrium. They also display clear outward signs of ovulation and fertility. They are typically only sexually active during the estrous phase of their cycle, which is referred to as being “in heat”. This change in physiology and behaviour alters the behaviour of nearby males.
Human Female Sexual Behaviour
Relative to the estrous cycle, menstrual cycles are associated with only very. small fluctuations in sexual behaviour and sexual desire.
Secretion of androgen by human adrenal glands.
Human adrenal glands, which are present in men and women, secrete a small amount of androgens. However, some people’s adrenal glands secrete abnormally-large amounts of androgens, which can start either before or after birth.
Excess androgen signalling by adrenal glands in males
Has minimal effect, since their testes already secrete tons of androgens.
Excess androgen signalling by adrenal glands in females
Excess androgen signalling can cause some degree of masculinization of either the body or brain or both. If the condition is present at birth, it is congenital adrenal hyperplasia (CAH). Depending on the amount of androgen signaling during development, sex organs can become slightly masculinized. Brain anatomy and function can also be masculinized. Females with CAH have a higher likelihood of identifying as a man and being sexually attracted to women in comparison to other females.
Female Sexual Behaviour Neural Circuitry
By injecting transneuronal retrograde tracer in muscles responsible for lordosis response in female rats, researchres identified the important neural pathways: VMH –> PAG –> nPGi –> motor neurons in spinal cord.
Ventromedial nucleus of hypothalamus (VMH)
Large nucleus in the hypothalamus that plays essential role in female sexual behaviour
Ventromedial nucleus of hypothalamus (VMH) in rodents
Electrical stimulation of VMH facilitates female sexual behaviour. Injections of estradiol and progesterone directly into VMH also stimulates sexual behaviour, even in females whose ovaries have been removed. Female with bilateral lesions of VMH will not display lordosis, even if she is treated with estradiol and progesterone.
Male Sexual Behaviour Neural Circuitry
The important neural pathways for male sexual behaviour include:
mPOA –> PAG –> nPGi –> motor neurons in spina cord
Male Preoptic Area (mPOA)
Nucleus in the anterior hypothalamus that plays essential role in male sexual behaviour. Electrical stimulation of mPOA in rodents elicits male copulatory behaviour. Within the mPOA, there is an area called the sexually dimorphic nucleus (SDN) of pre optic area. This nucleus is much larger in males than in females.
Pair Bond Formation
In approximately 5% of mammalian species, sexually mature couples tend to form long-lasting, fairly monogamous pair bonds. Some species of prairie voles form long-term pair bonds. Some don’t.
The formation of pair bonds seems to r elate to two peptides in the brain
Vasopressin and oxytocin. These compounds are released as neuropeptides in the brain and as hormones in the blood. Levels of them are elevated during sex, childbirth, and breastfeeding. The prairie vole
Prairie vole species
Form long term pair bonds. Have more vasopressin and oxytocin receptors in their ventral forebrain than other species do. Pharmacologically blocking or activation these receptors influences who they pair up with and when. Artificially increasing the expression of these receptors in non-monogamous prairie vole brains causes them to form life-long, monogamous-ish pair bonds.
Falling in love / becoming a drug addict
To ensure that we attain critical biological goals, specific brain circuits determine how valuable things are to us. Love and addiction do not affect overall intelligence; they skew priorities and choice behaviour. The brain areas that mediate these decisions and set priorities regulate our motivational processes and feelings of pleasure and happiness.
Electroencephalogram (EEG) in sleep
We measure brain activity by attaching electrodes to the scalp to record an electroencephalogram (EEG).
Electromyogram (EMG)
We measure muscle activity by attaching electrodes to the chin to record an electromyogram (EMG).
Electro-oculogram (EOG)
Electrodes are also placed near the eyes to measure eye movements via an electrooculogram (EOG).
Beta activity
13-13 Hz; typical of an aroused state. It reflects desynchronous neural activity (high frequency, low amplitude oscillations)
Alpha activity
8-13 Hz; typical of awake person in a state of relaxation
Theta activity
4-8 Hz; appears intermittently when people are drowsy, and is prominent during early stages of sleep.
Delta activity
<4Hz; occurs during deepest stages of slow-wave sleep; reflects synchronized low frequency, large amplitude brain activity.
Rapid eye movement (REM) sleep
Also called paradoxical sleep. Is associated with desynchronized EEG activity, rapid eye movements, dreaming, and muscle paralysis; muscles are totally inactive apart from occasional twitches. Cerebral blood flow and oxygen consumption increase.
EEG during deep sleep: slow-wave sleep
Stages 3/4 non-REM sleep (also known as deep sleep): corresponds to large amplitude, low frequency oscillations of brain activity as measured with EEG. This pattern of neural activity reflects synchronized bursts of action potentials in large collections of neurons.
REM Deprivation Studies on Animals
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.
Large developmental differences of sleep in humans
Newborns sleep 16 hours a day (50% REM / 50% NREM).
Adult humans sleep 7 hours a day (25% REM / 75% NREM).
Correlations: Sleep & Body. Weight
The amount of time a species sleeps each day is inversely correlated with weight. (Less sleep = Higher Body Weight).
Correlations: Metabolic Rate & Body Weight
While overall metabolic rate increases as mass increases, metabolic rate per pound (or per cell) decreases as mass increases.
Correlations: Metabolic Rate & Sleep
Higher body mass, higher brain mass, higher overall metabolic rate but lower metabolic rate per kg, lower heart rate, higher life span, lower total sleep time, higher length of sleep cycles.
Why do the corrections of metabolic rate & sleep exist
One hypothesis is that because 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.
Main Theories of Why Animals Sleep: To recover from physical or mental exertion
If the function of sleep is to recover from physical or mental exertion, then the amount of time spent exercising and thinking should correlate with total sleep time. However, the amount of sleep people get does not correlate very well with how much or little they exercise or study.
Main Theories of Why Animals Sleep: Brain Processing (learning and memory)
How can the brain update synaptic weights while it is currently operational and constantly receiving new information? Sleep give the brains the brain an opportunity to reorganize data and archive memories, which perhaps cannot be done efficiently while awake. Synaptic modifications clearly. occur during sleep. Learning and memory are impacted by sleep. During sleep the brain appears to be actively processing information and transferring it between different areas.
Main Theories of Why Animals Sleep: Waste removal
Since total sleep time correlates with body. size (as well as brain size, metabolic rate, heart rate, and life span), maybe it is critical for a process that benefits from economies of scale, such as nutrient use or waste removal. It seems that the clearance of proteins and waste products from the brain is almost nonexistent during wakefulness but really high during sleep. When animal sleep, glial cells in the brain seem to lose water and shrink in size - this increases the total volume of interstitial space, which promotes diffusion of cerebrospinal fluid through the brain, clearing away waste.
Glymphatic system
Removes excess proteins and other waste from the interstitial space of the brain. It regulates the process in which Cerebrospinal fluid (CSF) circulates around the brain and diffuses into it, into the interstitial space, thus becoming the extracellular solution that surrounds neurons. As CSF moves through the interstitial space, it clears waste products away before exiting into blood vessels.
Circadian Rhythm
There are many changes in behaviour and physiology that follow a 24-hour cycle. Controlled by internal biological clocks that continue to run in the absence of light, but daily variation in light levels keep the clock adjusted to 24 hours.
Circadian Rhythm of Rats
Rats are normally active at night. If we shift the light by a couple hours, they quickly adapted to this change. If the light is constantly dim, rats largely maintain their circadian rhythms, but they drift slightly over time. In continuous dim light, a brief pulse of bright light can shift their internal clock.
Suprachiasmatic Nucleus (SCN)
The SCN of the hypothalamus regulates circadian rhythms. It receives a direct input from the retina. Lesioning the SCN dramatically alters circadian rhythms (such as sleep-wake-cycles and hormone secretions). SCN lesions alter the length and timing of sleep-wake cycles, but they do not change the total amount of time that animals spend asleep.
What makes the clock of SCN neurons “tick”?
Circadian rhythms are maintained by the production of several genes and two interlocking feedback loops. When expression of one protein gets high enough, it inhibits its own production and promotes the expression of a different protein.
Advanced sleep phase syndrome / Delayed sleep phase syndrome
Advanced: mutation of a gene called per2 (period 2) causes a 4-hour advance in the biological clock (rhythms of sleep and temperature cycles) - a strong desire to fall asleep at 7pm and wake up at 4am. Delayed: a mutation of a gene called per3 causes a 4-hour delay in rhythms of sleep and temperature cycles - a strong desire to fall asleep at 2am and wake up at 11am.
The Sleep Molecule Hypothesis
What determines how much an animal needs to sleep? Consistent with the waste removal theory of sleep, there is a build-up of many molecules in the interstitial fluid of the brain during waking hours. These molecules are generally cleared away during sleep. Some of these molecules promote drowsiness and sleep at high concentrations.
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 signalling throughout the brain. Caffeine is an adenosine receptor antagonist.
Physiological mechanism of sleep and waking
Many neural circuits regulate arousal. Their activity is influenced by SCN neurons as well as the build-up of sleep-promoting molecules.
Wake promoting signalling molecules
Serotonin (raphe nuclei in the hindbrain), norepinephrine (locus coeruleus in the hindbrain), acetylcholine (throughout the brain), orexin (hypothalamus), histamine (hypothalamus).
Serotonin (5-HT) neuron activity
Positively correlates with cortical arousal (as measured by EEG), and drugs that increase serotonin signalling tend to suppress aspects of REM sleep (without affecting memory).
The Sleep/Wake Flip-Flop Circuit
Neurons in the ventral lateral pre optic area (vIPOA) of the hypothalamus promote sleep. Electrical stimulation of this are causes drowsiness and sometimes immediate sleep. Lesions suppress sleep and cause insomnia. vIPOA nueorns inhibit wake-promoting neurons, but this era receives inhibitory inputs from the same regions it inhibits. This kind of reciprocal inhibition characterizes a flip-flop circuit; both regions cannot be active at the same time and the switch from one state to another is fast. The animal is awake when the arousal, wake-promoting system is more active than the vIPOA neurons. The animal is asleep when vIPOA neurons are more active than the wake-promoting arousal system.
The Sleep Molecule Hypothesis: Adenosine Version
There are adenosine receptors on many neurons throughout the brain. Extracellular adenosine builds-up during the day. Sleep-promotong vIPOA neurons are activated by. adenosine signalling. Arousal-promoting acetylcholine (ACh) neurons are inhibited by adenosine signalling. The influence of adenosine signalling during the day can be masked by other regulators of sleep and arousal, such as SCN neuron activity. But at some point, when the clock of SCN neurons aligns with the build-up (or clearance) of sleep-promoting molecules, the whole network flip-flops and the animal transitions into (or out of) sleep.
Orexin (also known as hypocretin)
A peptide produced by neurons in the lateral hypothalamus (LH). Orexin neurons activity promotes wakefulness. Motivation to remain away activates orexin neurons. Most forms of narcolepsy are associated with the absence of orexin neurons.
Narcolepsy
A rare sleep disorder characterized by periods of excessive daytime sleepiness and irresistible urges to sleep, often with the other symptoms described below. The disease is related to the death of orexin neurons in the hypothalamus. they seem to be attacked by the person’s own immune system, usually during adolescence or young adulthood. Other symptoms include sleep paralysis and cataplexy.
Sleep paralysis
When REM-associated paralysis occurs just before a person falls asleep or just after they wake up. It is often accompanied by vivid, dream-like hallucinations.
Cataplexy
When complete muscle paralysis suddenly occurs when someone is awake. It is typically precipitated by strong emotional reactions or sudden physical effort (laughter, anger).
Insomnia
Characterized as difficulty falling asleep after going to bed or after awakening during the night. Affects approximately 25% of population and 9% regularly.
Fatal Familial Insomnia & Sporadic Fata Insomnia
A very rare disease that involves progressively worsening insomnia, which leads to hallucinations, delirium, confusional states, and eventually death (within a few years). Typically associated with progressive neurodegeneration around the thalamus, hypothalamus, and/or brain stem.
Disorders associated with non-rem sleep (non-rem parasomnias)
Disorders that occur during non-REM sleep or during transitions out of sleep. The brain seems to get caught between a sleeping and waking state. Most people are unaware they exhibit this behaviour. Sleepwalking, sleep-talking, sleep-groaning, sleep-crying, sleep-eating, sleep-teeth grinding, sleep terrors.
REM sleep behaviour disorder
Neurological disorder in which the person does not become paralyzed during REM sleep and thus acts out dreams. Appears to be a neurodegenerative disorder with at least some genetic component. It is often associated with more common neurodegenerative disorders such as Parkinson’s disease.
Learning & memory
Learning refers only to the process by which experiences change our nervous system and hence our behaviour. These changes are memories (memory traces or memory engrams). Memories can be transient or durable, explicit or implicit, personal or impersonal.
Cellular basis of long-term memory
Neuronal plasticity, which. refers to the ability of the nervous system to change and adapt.
Intrinsic excitability
When studying neuronal plasticity, researchers measure intrinsic excitability. It is the number of action potentials a neuron exhibits in response to depolarizing current injections. Can be measured with brain slice recordings.
Synaptic strength
When studying neuronal plasticity, researchers measure synaptic strength. It is the size of the response in a postsynaptic neuron when a presynaptic neuron has an action potential. A change in synaptic strength is called synaptic plasticity. Can be measured with brain slice recordings.
Measurement of Intrinsic Excitability
We measure intrinsic excitability by injecting depolarizing current into a neuron and counting the number of action potentials it has. Neurons with fewer potassium leak channels are more excitable.
Synaptic Plasticity
Changes in the strength of the synaptic connection between two neurons. If the postsynaptic response is depolarization, we call it an EPSP (excitatory postsynaptic potential).
Presynaptic changes of synaptic plasticity
There can be changes in the number of vesicles, the filling of vesicles, or the release of vesicles.
Postsynaptic changes of synaptic plasticity
There can be changes in the number of receptors, their sensitivity to neurotransmitter, and their response to neurotransmitter binding.
Habituation of Aplysias
Aplysia is an invertebrate sea slug with a simply nervous system. It has a large gill for breathing, and a siphon through which it expels water and waste. They reflexively withdraw their gill whenever their siphon is touched. Repeated light touches of the siphon reduce the magnitude of the gill withdrawal reflex to the point where light touches are ignored. This is an example of habituation.
Non-associative learning: Habituation & Sensitization
Habituation: reduced physiological or behavioural responding to a repeated stimulus.
Sensitization: when exposure to a strong stimulus (often painful) results in heightened responses to other stimuli.
After habituation, is the sensory neuron less sensitive to touch?
No, it depolarizes the same amount in response to touch before and after habituation.
After habituation, is the sensory neuron less excitable in general?
No, the same amount of depolarization is needed to elicit an action potential before & after habitation.
After habituation, is the connection between the neurons weaker?
Yes, when the sensory neuron spikes, there is a smaller response in the motor neuron
After habituation, is the motor neuron less excitable in general?
No, it spikes the same as before when depolarized a set amount
After habituation, is the connection between the motor neuron and gill weaker?
No, the gill is just as sensitive to an action potential in the motor neuron as before.
Long-term potentiation (LTP)
Strengthen synaptic connection. High Frequency (100Hz/s). Increase synaptic strength in postsynaptic neuron. Number of receptors and amount of vesicles and nitric oxide goes up.
Long-term depression (LTD)
Weaken synaptic connection. Low Frequency (1Hz/10 minutes). Decrease synaptic strength in postsynaptic neuron. Number receptors and amount of vesicles and endocannabinoids goes down.
Why do the same number of stimulations that produce LTP also produce LTD at a slower rate
They are a function of the number of times the synapse is activated as well as whether the postsynaptic neuron fired action potentials at those precise time.
Long-term potentiation
Synaptic strengthening occurs when synapses are active while the membrane of the postsynaptic cell is depolarized.
The NMDA receptor: A coincidence detector
A unique type of ionotropic glutamate receptor. Opens when it binds glutamates ut magnesium (Mg2+) easily get stick in the pore of this ion channel and block all current flow. This blockage only occurs when the membrane potential of the cell (where the receptor is) is hyperpolarized (<-40mV), like when the cell is at rest. When the membrane of the cell is slightly depolarized, Mg2+ ions won’t try to pass through NMDA receptor, and so won’t clog the pore. So, flow through NMDA channel is gated by both glutamate binding and membrane potential of the cell.
AMPA receptor
The ionotropic glutamate receptor that mediates most the fast excitatory synaptic currents in the brain. It lets in sodium ions when open, causing EPSPs and membrane depolarization.
CaMKII
Type II calcium-calmodulin kinase. It is an enzyme that is activated by calcium influx through NMDA receptors. IT participates in the intracellular signalling cascade that establishes long-term potentiation at glutamate synapses, by increasing the number of AMPA glutamate receptors in the postsynaptic membrane.
Growth of dendritic spines after long-term potentiation
For glutamatergic synapses that form on dendritic spines, the strength of the synaptic connection correlates with the size of the spine and the number of AMPA receptors in it. It is relatively easy to measure changes in the sizes of spines over time. The size of many spines is is constantly in flux, but some spines are very stable.
Associative long-term potentiation
The increase in synaptic strength that occurs in weak synapses that happen to be active when stronger inputs get the postsynaptic neuron to spike. If the weak stimulus and strong stimulus are applied at the same time, the synapses activated by the weak stimulus will be strengthened.
Synaptic plasticity: Hebb’s rule
Hypothesis proposed by Donald Hebb: The cellular basis of learning that involves the strengthening of synaptic connections that happen to be active when the postsynaptic neuron fires an action potential.
Steps of long-term potentiation
- Depolarization is sufficient to trigger action potential in axon of pyramidal cell.
- Action potential reaches terminal button of strong synapse: produces strong EPSP.
- Dendritic spike washes back along dendrite; primes NMDA receptors in dendritic spines
- Action potential reaches terminal button: glutamate is released
- Long-term potentiation: synapse is strengthened
Sensory memory
Initial sensation of environmental stimuli
Short-term memory
Limited to a few items. Tips for longer time: rehearsal and chunking
Long term memory
Relatively permanent, consolidated STM to LTM
Unconscious Memory (Non-declarative)
Implicit, procedural. Do not require conscious retrieval (operate automatically). Motor learning, perceptual learning, classical conditioning.
Consciously accessible memory (Declarative)
Explicit, declarative. Memory of events and facts. Episodic: Recollection of specific episodes, including time, space context. Semantic: Facts, general information without context.
Perceptual Learning
Pattern recognition system: enable to recognize & identify objects. People can recognize changes in familiar stimuli. Neocortex. Implicit memory.
Motor Learning
Learning to make a sequence of movement. Get feedback from joints, eyes, ears, etc –> improve & optimize. Cerebellum, thalamus, basal ganglia, & motor cortex. Implicit memory.
Relational Learning
How distinct perceptual objects relate to each other: describe the scene. Stimulus-stimulus learning (relationships among stimuli). Hippocampus: covert short-term to long-term memories, dysfunctional hippocampus –> cannot get new declarative memory. Declarative memory (semantic & episodic) –> explicit.
Stimulus-Response Learning
Learning to perform particular behaviour when particular stimulus is present: establish connection between perceptual and motor circuit. Operate conditioning: form of learning in which a reinforcing or punishing outcome follows a specific behaviour in a specific situation.
Classical Conditioning (Pavlovian Learning)
Association between two stimuli (unconditioned and conditioned):
1) Unconditioned stimulus evoke reflexive behaviour
2) When CS and US presents at the same time repeatedly
3) When CS evoke reflexive behaviour without US, then we call it classical conditioning –> we call response by CS only as CR
Associative Learning - Rat and air puff
Play a tone every time you blow the air puff into the eye of rat. Later mouse will associate tone and air puff. Then it close its eye without air puff when tone plays (classical conditioning).
Hebb’s Rule: Fire together, Wire together
When neuron 1 is activated by air puff, it depolarizes post synaptic cell. When neuron 2 is activated by tone at the same time –> post synaptic cell was already depolarized –> LTP occurred –> Synapsed will be strengthened.
Operant conditioning (instrumental conditioning)
Learning from the consequence of actions: reinforcement (increase behaviour), punishment (decrease behaviour), positive (get something), negative (remove something). Step: exploratory behaviour (don’t know the consequence - animal’s decision), result from exploratory behaviour, change the likelihood of action.
Neural circuit of instrumental conditioning
Direct transcortical connections: cerebral cortex to other area, behaviour with consciousness. Basal ganglia (collection of nuclei in forebrain): behaviour become habitual response (without conscious, automatic) based on the result & repeated behaviour. Striatum: synapse strengthen based on dopamine. Dopamine indicates the animal’s motivation or value of result.
Amnesia
Memory deficit caused by brain damage or disease. Anterograde amnesia: inability to learn new information after disease, but hey have intact memory before disease - Korsakoff’s syndrome & confabulation. Retrograde amnesia: inability to remember events that occurred before disease.
