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PSYCH 223 Prelim 2 Study Questions


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Development of the nervous system in the human embryo and fetus
At 18 Days
-the embryo has begun to implant in the uterine wall.
-it consists of 3 layers: endoderm, mesoderm and ectoderm.
2) A thickening of the ectoderm leads to the development of the neural plate.
3) At 20 days, the neural groove begins to develop.
4) At 22 days teh neural groove has closed to form the neural tube.
5) At 24 Days, four major divisions of the brain (telencephalon, diencephalon, mesencephalon and rhombencephalon) are discernible.
central canal
is what develops into the ventricle system
spina bifida
when the neural tube fails to close on the spinal end.

-pasrts of teh spine and spinal cord are exposed, and it is associated with paraplegia.
when the neural tube doesn't close on the brain end.

-the person essentially does not develop a brain. It is invariably fatal and is the cause of many stillborn infants
stages of neural development
-neurons are born around the central canal and begin to stretch outwards.
2) neural migration
-the neurons migrate outwards from the central canal towards the surface.
3) differentiation
-neurons arrive at their desitnation and differentiate into different types of neurons.
4) synaptogeneisis
-the estaphlishment of synaptic connections as axons and dendrites grow
5) neuronal cell death
-the selective death of many nerve cells
6) synaps rearrangement
-the loss of some synapses and development of others, to refine synaptic connections.
growth cones
enable axons and dendrites to reach their targets. The cones are able to sens chemicals--either chemoattractants or chemorepellants--from target cells, which direct the cones where to go.
-located at the tip of both axons and dendrites.
-the filopodia and lamellipodia extend from the growth cones and adhere to the extracellular environment, and then they contract to pull the growth cone in a particula direction
neurotropic factors
-promote the health of the neurons that pick it up.
-neurons and individual synapses compete for neurotrophic factors. those that win saty healthy, but those that lose die out.
-neurotrophic factors allow neurons to survive and grow

--becuase the amount of neurotrophic factor matches the number of target cells, this process results ina arough matching of the size of the target and the number of innervating neurons.

-p. 196
synapse rearrangement
there is an over-production of synapses followed by pruning.
-Active synapses are preserved, and less active synapses are pruned.
p The density of synapses declines after the first year.
experience-dependant plasticity
rats in an impoverished vs. enriched condition

Experience-dependent processes: neuronal connections are made
that reflect the unique experiences of an individual
experience-expectant plasticity
the nervous system develops so that it's ready to accept input and be modified accordingly.
ex) the 3 eyed frogs.
-the development of the visual cortex in frogs depends on the type of visual stimulation it receives.

-a particular experience that is expected in the environment contributes to the wiring of that system.

Experience-expectant processes involve species-typical
information. According to these processes, synapses are formed
and maintained when an organism has species-typical experiences,
will develop for all members of a species, given a species-typical

--Prewired for specific experiences and to develop certain abilities, but still influenced by experience
binocular deprivation
-is an example of experience-expectant plasticity
-can lead to blindness and abnormal connectivity of neurons.
monocular deprivation
--depriving one eye

--causes profound abnormalities in the wiring of the visual system
ocular dominance columns
-not only do the columns receive input from a certain orientation, but also from either the right eye or the left eye.

-all at the level of V1.
a common situation where there is misalignment of one eye

-lazy eye

-one eye doesnt compete well for cortical influence

-if left alone, the eye will go blind due to lack of stimulation.

-by placing an eye patch over the strong eye, you force the other eye to work and form connections.

-there is a sensitive period in humans a\lso, so if you wait too long (past 10 years old) you can't repair the condition.
Fragile X syndrome
-is the most common form of inherited mental retardation.

-is 2x as common in males as in females

-can cause autism.

-is due to additional repeats on the 23rd chromosome, which is why girls are much less susceptible. Males only have one x-chromosome, so if they are afflicted they don't have another one to make up for it.

-results in a failure to manufactore FMRP. the lack of this protein causes the syndrome.
FMRP knockout mouse
-early in development, there is no difference between control mouse and the fragile x mouse.

-later, the control mice have FEWER dendritic spines.

-fragile x mice didn't prune back the surplus connections. Also, the dendritic spines were immature in the fragile x mice.

-dendritic spine abnormalities have also been found in humans with fragile x syndrome.

-some studies have found an enlargement of some brain regions in fragile x which may suggest that extra tissue was not pruned back,

-emphasizes that EFFICIENCY OF CONNEcTIVITY is important, not just raw numbers or sheer volume.
autism (Autistic Sectrum Disorders)
deficits in:
-social interaction****
-verbal and nonverbal communication
-repetitive behaviors or interests (rocking motions, etc.)
-cognitive deficits (not in all cases)
-impaired theory of mind.
-difficulty interpreting social cues (facial expressions, tone of voice)
-may appear indifferent to people,
-don't smile
onset of ASD
-some children with ASD exhibit behavioral abnormalities from birth, while others can exhibit normal development for many months, and even 3 to 4 years in some rare cases.

-this is followed by sever decline in functioning: a loss of language, social withdrawal.
neorological bases of ASD
-abnormalities in face processing
ex) normal subjects, when looking at faces, exhibit a highly stereotyped pattern of looking at the eyes and then down to the mouth.

-autistic patients had extraordinarily different gaze preferences.

-there is an enlargement of some brain regions.

-the neurons are smaller and more numerous in some limbic regions

-there are more dendritic spines in the cortical neurons. This suggests a possible pruning failure.

-there is increased activity in some regions and decreased activity in other regions.
Belmont's theory on neural connectivity
-Connections in unaffected subjects are limited within local areas and strong between distant areas.

-The LAYOUT of the connections is what matters, not the number of connections.

-with autistics, there is high local connectivity and low long-range connectivity
-may lead to poor signal-to-noise ratio and heightened sensitivity to stimuli.

-the poor long-range connectivity may lead to impaired integration of information.
fetal alcohol exposure (effects)
-facial deformities, -impaired cognitive functions
-problems with learning, memory, attention
-mental retardation
-motor impairments
time of exposure and FAE
WHEN the subject is exposed to alcohol makes a big difference on the severity of the effects.

-early exposure is related to bodily malformations

-exposure in the third trimester can be extremely devastating to the brain.
effects of fetal alcohol exposure in the rat model
-interference with neurogenesis
-disruption of radial glia, preventing neural migration
-disruption of NT systems which are important for stabilizing synapses in development.
-disruption of cell adhesion molecules, which are important for synaptic connectivity.
FAE and the cerebellum
FAE causes a massive loss of Purkinje neurons.

-loss of Purkinje neurons results in poor coordination, motor skill deficits, etc.
FAE rehabilitation
-the alcohol-exposed rats were severly impaired, but motor skill traiing brought their performance into the normal range.

-alcohol killed the Purkinje neurons, but motor skill training induced synaptogenesis.

-rehab didn't regrow Purkinje neurons, but it improved their connectivity by increasing the number of synapses on the remaining neurons.
is about collecting data about what's going on in the external world
-is the study of how the brain puts all the bits of sensory info together into a coherent percept or idea.

-is influenced by the information you bring to the situation.
ex) you think line AC is longer because of your knowledge of depth perception.
labeled lines
the brain knows what kind of sensory info its getting by what line it comes in on.
-is a "joined sensation"

ex) music sounds may be perceived as shards of colored glass

ex 2) letters and numbers can evoke color perceptions.
predispositions to synesthesia
-occurs most commonly in females and non-right handers
-seems to be hereditary
-co-occurs with good memory, but poor math and navigational skills
possible causes of synesthesia
1) local cross activation
-ex) the visual word form area is adjacent to the color area of the cortex, and activity can be found in both areas of synesthetes.

-could be a possible pruning failure.

OR it could be caused by feedback from multi-sensory areas
receptor cells
-involved in sensory transduction

-convert energy from the outside world into neural energy (membrane potentials)

-the kind of energy that activates a receptor cell depends on the shape and characteristics of that receptor.

-receptors transduce info from the external world into a code the brain can understand (action potentials)
-convert light into membrane potentials
convert chemical energy into membrane potentials
ex) tastants and odorants
convert mechanical energy
Pacinian corpuscles
-detect vibration (mechanical stimulation)

-the nerve ending is enclosed in a layered structure.

-if you push on the structure, the membrane stretches, which opesn NA+ channels

-this causes depolarization and generates an action potential
simple rate code
codes the intensity of a stimulus.

-if the neuron is firing fast, it is a big stimulus.

-if the neuron is firing slow, it's a small stimulus.

-this method is limited because of the refractory period between action potentials
range fractionation
-different neurons have different threshold levels.

-therefore, different neurons respond to different intensities.

-if only low receptors fire, you know it was a low-intensity stimulus

-if low and medium receptors fire, you know it was a medium intensity stimulus
temporal pattern codes
a stimulus can be identified by the patter of firing by a given neuron (like Morse code) or across many neurons
how do you know where a stimulus is?
-sensory systems are highly organized.

-the somatosensory topographic maps, for example.
phasic responses
-fast adapting
-allows you to focus on CHANGES in the environment, which are more evolutionarily relevant.

tonic responses
show a slow or nonexistent decline/adaptation.
center-surround receptive fileds
-the neuron fires when you touch it right ni the center, but there is a suppression of activity just outside the center.

-plays a critical role in detecting edges
levels of sensory processing
-peripheral nerves-->spinal cord-->brainstem-->midbrain-->thalamus-->primary sensory cortex-->nonprimary/secondary sensory cortex
top-down processing
-hgiher cognitive centers influence the way info. enters the brain and is perceived.

-your prior beliefs, adaptations and cognitions influence how you perceive things.
Pacinian coruscles
-detect vibration (mechanical stimulation_

-the nerve ending is enclosed in a layered structure

-if you push on the structure, the membrane stretches, which opens Na+ channels.

-this causes depolarization and generates (sometimes) an action potential
temporal pattern coding
a stimulus can be identified by the pattern of firing by a given neuron (like Morse code) or across many neurosn
center-surround receptive field
neuron fires if you touch the center of the receptive field, but response is suppressed if you touch the surround.

-plays a critical role in detecting edges
plasticity in sensory systems
-somatosensory and motor cortices can reorganize themselves based on experience.
how do we feel pain?
1) damaged tissue releases chemicals

2)chemicals excited nociceptors on free nerve ends.

3) this sends pain info thru the spine (by way of the dorsal horn of the spinal cord) and to the brain

4) pain fibers release glutamate as a transmitter and substance P as a neuromodulator. in the spinal cord
c fibers
-small, slow, unmyelinated

-respond to cold, dull pain, and moderate heat
a-delta fibers
-fast and myelinated
-rspond to sudden pain, heat
-both carry pain info
cingulate cortex
-is especially activated by pain info.
descending pain modulation pathways
periaqueductal gray neurons release endorphins-->raphe Neurons release serotonin--->spinal neurons-->endorphins are released to inhibit the spino-thalamic neurons carrying the pain signal
chemical senses
are the evolutionarily oldest senses.

-can be highly developed
pathway in the olfactory system****
1) odorants get stuck to the olfactory epithelium

2) olfactory ephithelium connects to the olfactory bulb.

3) olfactory bulb sends info to the hippocampus.


-olfactory cells can be regenerated.
the vomeronasal organ
-is related to the olfactory system.

-is used for the detection of pheromones.

-researchers are not 100% sure whether or not humans have a VNO

-seems that the genes for it are inactive in humans, but evidence of women living together having concurrent menstrual cycles suggests otherwise.
what is sound?
-vibrations in the air

-the compression and expansion of air molecules which can be represented as a sine wave.
height of a wave

-determines the volume of a sound.

-larger amplitude=louder sound.
-how fast the wave cycles.

-determines pitch.

-faster frequencies have a higher pitch.
-outer ear

-its shape physically transforms sound energies to modify the character of sound that reaches the middle and inner ear.
middle ear
-is made up of ossicles and the tympanic membrane (eardrum).
the ossicles
-3 tiny bones:
-malleus, incus, and stapes.

-it transmits vibrations in the air to the oval window, the divider between the middle ear and the inner ear.

-the ossicles can contract to protect the inner ear from damaging loud sounds.

-muscles of the inner ear control sensitivity.
conduction deafness
-a failur of the transmission of vibrations in the air to the cochleuss where transduction takes place.
inner ear
-made up of the cochlea and canals

-converts sound into neural activity.
-has a snail shell shape.

-is a coil of three parallel, fluid-filled canals.
three canals in the cochlea
-vestibular canal, middle canal, and tympanic canal
transmits vibrations to the inner ear via the oval window.
round window
separates the tympanic canal from the middle ear

-has a moveable membrane.

-when the oval window receives a vibration, the round window membrane stretches to allow fluid vibration.
organ of Corti
-sits on the basilar membrane of the cochlea

-contains hair cells and terminations of the auditory nerve.

-is composed of the primary components that do the work ofconverting sound energy into neural activity.

-has 3 main structures:
1)hair cells 2)supporting cells 3)terminations of auditory fibers

-base of the organ of corti is the basilar membrane
hair cells
-2 types: inner hair cells and outer hair cells

-have stereocilia on their ends

-the stereocilia are embedded in the tectorial membrane, which is attacted to Reissner's membrane.
what happens when the basilar membrane moves?
-the tectorial membrane and the organ of Corti slide against each other-->causes a slight bending of the hairs-->causes the sensation of sound
1) sound comes in through the pinna
-the "hills and valleys" of the pinna physically transforms sound energies to modify the character of the sound that reaches the middle ear. It amplifies some frequencies and dampens others.

2) Goes thru tympanic membrane to the middle ear.
-the ossicles (made up of the stapes, incus and malleus) transmit vibrations in the air to the oval window. The middle ear muscles control the ossicles and can contract to move the ossicles to protect the inner ear from potentially damaging sounds.

3) The oval window stimulates the round window, which separates the middle ear from the tympanic canal in the inner ear. When the round window receives a vibration from the oval window, the round window membrane stretches to allow fluid vibration in the cochlea.

4) Sound pressure entering the liquid of cochlea generates a
traveling wave along the basilar membrane

5)Vibration of the basilar membrane causes bending of
stereocilia and this opens ion channels which modulates
potential within the cell
⬢ Activation of the cell releases neurotransmitter to
synaptic junctions between hair cell and neural fibers of
the auditory nerve
⬢ A neural spike is generated that propagates in the
auditory nerve fiber

pinna--->ossicles (stapes vibrates)-->vibration of the cochlear fluid-->causes vibration of the basilar membrane-->hair cells on the basilar membrane are stimulated-->inner hair cells-->afferent nerve fibers to the cochlear nucleus in midbrain-->goes to the superior olivary nuclesus-->inferior colliculus-->medial geniculate nucleus-->auditory cortex
tip links
fine, threadlike fibers that are attached to K+ channels at the tips of the stereocilia (hair cells).

-when the hair cell is stimulated, they're the ones that open the ion channels.
basilar membrane
-a membrane in the cochlea that contains the principal structures involved in auditory transduction (i.e. hair cells).

-is the base of the organ of Corti

-separates the tympanic canal from the middle canal.

-vibrates in response to souond

-is wider at the top of the cochlea than at the bottom

-different parts of the basilar membran are affected by different frequencies of auditory stimulation.

-the membrane exhibits distinct "tuning"

-high frequencies cause the basilar membran to vibrate most near the cochlear base

-hair cells attached to the basilar membrane are stimulated depending on where they are attached and depending on the frequence of sound.
inner hair cells
-located within the organ of corti.

-make up 90-95% of auditory fibers to the brain.

-are flask shaped.

-afferent nerve fibers running from IHCs are responsible for sound perecption.
outer hair cells
-are responsible for modulating acoustic stimulation.

-can change their length, causing segments of the basilar membrane to stiffen or relax, thus actively sharpening its tuning to different frequencies.

-tunes in to different frequencies.

-can inhibit loud sounds

-when they tighten, they pull the basilar membrane closer to the tectorial membrane, dampening noise.

how is sensation an active process?
-the OHCs stiffen when depolarized, causing the basilar membrane to change its stiffness and allows for tuning and dampening of loud noises.
tonotopic organization
-a feature in the auditory systems in which neurons are arranged as an orderly map of stimulus frequency.

-cells responsive to high frequency are located a distance from cells that respond to low frequency.
place theory
-states that you identify the pitch according to which IHCs are stimulated (i.e. which part of the basilar membrane is most vigorously vibrated).

-tries to describe auditory coding and how auditory info is coded so that we can perceive particular sounds.

-the problem with this is that you never hear one pure tone at a time so there are vibrations in multiple areas. There are often a mixutre of which areas are stimulated at once.

-high pitches usually use the place theory more.
volley theory
-states that you identify the pitch according to the firing rate of incoming action potentials.

-a rate code is used--for example a 500 Hz tone results in 500 action potentials per second.

-problem: neourons can only fire for a maximum of around 1000 Hz because of the refractory period.

-low pitches usually utilize the volley theory more
auditory coding
-a combination of both place theory and volley theory is used, which is how people can code for frequencies higher than around 1000 Hz.
sound localization
-is encoded through intensity differences, because the sound source will be more intense in the ear on the same side as the stimulus.

-latency differences are differences between the two ears in the time ofarrival of sounds.
binaural latency detection
-if the sound arrives at both ears at the same time, the stimulation will reach the same point at the same time

-if the sound arrives at the left ear before the right ear, the sensations will meet at a neuron closer to the RIGHT ear.

-this indicates to the brain that the sound must be coming from the left.
binaural localizaton studies
-in owls, if visual images are displaced, then binaural localization will be displaced too.

-when a tone was played for owls that had lenses that shifted the image 10 degrees off, they looked 10 degrees off as well.

-eventually, the visual and auditory maps shift to compensate for the lenses.
noise-induced hearing damage
leaves car tissue on both the IHCs and the OHCs.
natural hearing loss
-starts with high-pitched tones.
cochlear implants
-when IHCs are not functional (or dead), hearing can still be restored to some degree.

-even though the hairs aren't there, the axons still are.

-cochlear implants are transmitters behind the ear that are surgically implanted in the cochlea.

-using the implanted electrodes, they selectively stimulate nerves in different regions of the cochlea.
cochlear implants vs. hearing aids
-hearing aids are just amplifiers.

-with hearing aids, everything is amplified, including background noise.

vestibular system
-largely responsible for balance.

-provides info about the force of gravity on the body and the acceleration of the head.

-informs the brain about mechanical forces that act on the body.

-partially made up of three semicircular canals that are filled with fluid, as well as the the utricle, the saccule and ampullae.

-receptor hair cells are found in the ampullae, the utricle and the saccule, where they are embedded in a gelatin.

-vibrating or moving fluid casues the cilia to bend.
-small, bony crystals on the gelatinous membrane that add mass to the layer to make it more sensitive to movement.
-a part of the vestibular system that is sensitive to horizontal linear acceleration.
-part of the vestibular system that is sensitive to vertical linear acceleration.
semicircular canals
-are sensitive to changes in direction.
motion sickness
-can be caused by disagreement among sensory systems, like when the vestibular and visual information conflict.

ex) when reading in the car, your visual system is focused on something that is not moving. However, you are actually moving very quickly.
visual system images
-images projected on the retina are upside down and backwards.

-the brain doesnt need to turn them around because it knows how it's wired.
pigmented epithelium
the outermost layer of the eye.

-in some animals, this is where reflectin is located, which is what causes their eyes to "shine" or reflect light in dim lighting.
visual pathway in the eye
-pigmented epithelium-->rods and cones-->bipolar cells-->ganglion cells-->optic nerve fibers.
-are used for dim light vision

-don't provide good acuity.

-part of the scotopic system (works at night)

-there are way more rods in the eye than cones.

-don't respond differently to different wavelengths.

-outside of fovea

-are highly sensitive, can be stimulated by weak amounts of light.

-used for night vision.

-receptive field is larger, so acuity is lower.

-slow temporal responses.
-color vision

-used for high acuity vision

-need lots of light.

-part of the photopic system.

-needs strong stimulation, used for day vision.

-concentrated in and near fovea.

-relatively rapid responses

-small receptive field=good acuity.
-rods and cones release neurotransmitter all the time.

-stimulation by a light source is indicated by STOPPING or REDUCING neurotransmitter release.

-light stimulates photopigment, which causes a 2nd messenger cascade that results in Na+ channels CLOSING and the cell becoming HYPERPOLARIZED.

-this "backwards" system tends to promote sensitivity, integration of signals over time, and adaptation.
-a photopigment found in rods that can be activated by a single photon of light.

-when light stimulates it, a second messenger system reduces cGMP and causes the Na+ channels to close.

-rhodopsin then breaks down into retinal and opsin.

-retinal and opsin must recombine before they can respond to light again.
receptor adaptation
-is critical for vision

-it allows the retina to process light intensities that differ by more than 1 billion times.

-photopigment levels are also a factor since it takes time for photopigments to recombine after being split by light.

-availability of retinal chemicals for transduction is also important since some chemicals are depleted during transduction and have to be replenished.
the fovea
-is the focal point at the back of the eye

-is the point of highest acuity.

-has lots of cones in it.

-as you move away from the fovea, there are fewer cones and more rods, which leads to low acuity but good dim light vision.

-high receptor density.
optic disc
-is directly beneath the fovea.

-it's a blind spot where the optic nerves leave the eye for the brain.
why look at a star indirectly?
-you'll see it better if you are not focused directly on it because the outer edges of the retina are better for dim light.
the periphery of the eye
-color vision and acuity drops off rapidly as you move away from the fovea.
receptive field
-consists of the stimuli in visual space that increase or decreases the neuron's firing.

-is what happens "upstream" from the receptors.
on center/off surround cell
-is stimulated by a stimulus in the center and inhibited by activation in the surround.

-a spot of light in both the center and surround causes intermediate activity since there is a combination of activation and inhibition.
lateral inhibition
-the phenomenon by which interconnect4ed neurons inhibit their neighbors, producing contrast at the edges of regions.

-this plays a role in receptive fields since when certain cells are "turned on" their neighbors are "turned off"

-interneurons, such as horizontal cells and amacrine cells are responsible for lateral inhibition.

-cells on the edge of the group are the most activated since they are only inhibited on one side.

-makes the edge pop out and is responsible for "edge detection"

-a light center with a dark surround is what yields the highest activity due to the least inhibition, and leads to better edge detection.

-the eye is NOT a light meter. it is actually an edge detector because of lateral inhibition.
from receptors to ganglion cells
-receptors are hyperpolarized when stimulated.

-this hyperpolarization leads to a DEPOLARIZATION of bipolar cells, which causes an increase of firing in ganglion cells.
from receptors to ganglion in off-center cells
-receptors are depolarized, and this causes depolarization of bipolar and depolarization/decreased firing rate of gaglion cells.
properties of connection between receptor and ganglion cells
-lot of convergence within this system, which helps to construct receptive fields.

-lots of photoreceptors link to a few horizontal cells or a bipolar cell-->ganglion cell
LGN receptive fields
the receptive fields of many retinal ganglion cells combine to form the receptive field of a single LGN cell.

-the receptive fields of many LGN cells combine to form the receptive field of a single VI cell in the cortex.
cortical neurons are sensitive to different kinds of input
-visual cells in the thalamus (LGN) have concentric receptive fields (on-center/off-surround)

-visual cells in the cortex may show orientation specificity or respond only to motion, etc.
"simple" cells
-respond to a bar of light or edge in a particular orientation.

-occurs through the process of convergence. (retina-->LGN-->thalamus)
"complex" cell
is sensitive to movement throughout the field.

-are like motion detectors.

-changing the angle slightly yields a weaker response
the black and white motion spiral
-the residual movement of the landscape process was due to opponent processes.

-when staring at a rotating picture, motion detectors for that direction get fatigued.

-those detectors that aren't fatigued take over which makes it look like it's moving in the opposite direction of the picture you were just watching.
anomalous motion
-depends on the differences in shading or color

-motion occurs in the periphery.

-direction depends on the direction of shading gradation.
3 components of color
1) brightness
2) hue
3) saturation
-describes the intensity of light
-is what most people mean when they use the word color.
-is how saturated wtih the color it is (faint vs. deep)

-yellow always appears more saturated than blue because it is a brighter color.
trichromatic theory of color vision
-there are three kinds of cones, and each respond to a different wavelength (color).

-however, the color ranges are wide and overlapping.

precise hue discrimination depends on the relative activity of different cones.

-the three receptor types don't respond uniquely to that one color, they just prefer it. Two out of the three types will respond to any kind of light, but they have different peaks of sensitivity.

-this alos for high visual acuity and the ability to see many different hues.
dim light vision
-during rod saturation, it is temporarily fatigued due to rhodopsin breaking down and having to join back together again.
opponent process theory of color vision
-there are three pairs of opposing colors (red/green, blue/yellow, black/white)

ex) stare at the flag and then see its after-image because those neurons are fatigued.
chromatic induction
-colors that are the same may appear different, and colors that are different may appear the same.

-the perceived color is influenced by the colors around it.

-the color appearance of light changes in the presence of surrounding light

-one aspect is assimilation. Color appearance changes in a direction towards the color of the surrounding light.

-induction and grouping also occur in which identical stimuli are perceived differently when they are part of structuresw that appear to be different.
missing S-cones
cannot distinguish blue hues
missing M or L cones
cannot pick out red hues.
bottom-up processing
-involves constructing a percept, piece by piece, from small details.
-photoreceptor cell is activated-->if rod and an on-center cell, activates cGMP-->cGMP hyperpolarizes the cell by closing Na+ channels-->this info. causes bipolar cells to become depolarized--->ganglion cells become depolarized-->axons leave eye through the optic nerves-->at optic chiasm, axons from the nasal side cross to the other side-->most go to the LGN in the thalamus-->primary visual cortex (V1)-->back to LGN for feedback.

-an especially large part of the primary visual cortex is devoted to the fovea.
columnar organization in V1
-the neurons in V1 are organized into columns, and each column responds to the same kind of stimulus.

-every neuron in the same column has the same orientation bias.

-therefore, they're called orientation columns.
-each column is a processing unit

-adjacent columns respond to stimuli that are similar, but slightly different from the stimuli that activate the column next to it.
visual processing stream
1) V1 neurons respond to edges of a particular organization.

2) V2 neurons respond to somewhat more complex stimuli, such as illusory contours.
ex) inclomplete shapes
2) v4 neurons respond to more complex stimuli
-those spinny shapes
3) V5 is specialized for motion perception
-if this area is damaged, objects appear to jump from position to position.
dorsal stream
-is responsible for appreciating where things are in the visual field.

is called the "WHERE STREAM"
ventral stream
-is responsible for visually identifying and recognizing objects


-lesions in the ventral stream impair object recognition, a condition called agnosia.
-inabiity to recognize objects.

-usually due to a lesion in the ventral stream.

-seems to be an inability to put details together to form a coherent precept.
optic ataxia
-can identify objects, but can't grasp them

-usually due to a lesion in the dorsal, or "where", stream.
object agnosia
-is an inability to recognize real objects.

-you can't tell what a rose is just by looking at it, but you can tell by smelling it.
drawing agnosia
-the inability to recognize drawn objects.
-an inability to recognize faces.
color agnosia
-an inability to associate colors with objects.
color anomia
-an inability to name colors.
-an inabiltiy to distinguish ues.
visual and spatial agnosia
-an inability to use stereoscopic vision
movement agnosia
-an inability to discern the movement of objects.

-moving objects appear to jump from location to location.
support for the "face processing module"
-prosopagnosia appears to be a selective deficit in face perception.

-there are neuronal responses that are selective for faces.

=you can influence perception by artificially activation the face processing area.
evidence agains the "face processing module"
-prosopagnosiacs often have difficulty recognizing other complex objects, not just faces.

-area IT seems to be involved in expert recognition of complex objects, not jsut faces.
ex) greebles
hemi-spatial neglect
-a deficit of attention to half (either the right or the left_ of the visual field.

-is often caused by lesions in the central sulcus.

-you can move objects to the deficient visual field, and the subject won't respond to them until they're in the working visual field.

-patients can se the objects in the neglected field (are not blind). They are just incapable of directing their attention to the object.

-result of some damage in both the dorsal and the ventral streams.
behavioral evidence for top-down processing
-once you see something, it's difficult to go back to the naive state.

-it is difficult to choose not to be influenced.
-higher cortical processing areas project back to lower cortical areas.
optic chiasm
-where the optic nerves cross the midline

-located just anterior to the stalk of the pituitary gland.
dorsal roots
serve sensory functions
ventral roots of the spinal cord
contain motor fibers
motor plan
complex movements and acts controlled and produced by a set of commands to muscles that is completely established before an act occurs.
-simple reflexes, are discrete, and often limited to a single body part
complex, sequential behaviors

-often goal-oriented

-act is a sequence of movements
closed loop control mechanisms
-known as "ramp movements"

-maximize accuracy

ex) driving a car

-continually guided by feedback.
open-loop control mechanisms
-maximize speed

-no feedback

-ballistic movements

ex)throwing a pitch
skeletal system
determines which movements are possible
spinal cord
controls skeletal muscles in response to sensory info

implements movement commands from the brain
integrates motor commands from higher levels of the brain and transmits them to the spinal cord.
connect muscles to bones
antagonist muscles
when one contracts, the other extends
synergist muscles
work together
sliding filaments
-how you move

-myosin binds to actin and bend to slide one past another

-this shortens the muscle
fast-twitch muscle fibers
-fast ands strong

-get tired easily


-"white meat"
slow-twitch muscle fibers

-slower, but less easily fatigued.

-innervated by small motoneurons

-are more easily excited
-excites muscles

-every action potential from a motoneuron causes a contraction in muscle fiber.

-only way to prevent a contraction is to inhibit the motoneuron
motor control
when each axon only innervates a few muscle fibers, you have fine motor contol
motor unit
-consists of a single motor axon and all the muscle fibers it innervates
innervation ratio
-ratio of motor axons to muscle fibers
final common pathway
-motoneurons are the final common pathway that links activity from the rest of the spinal cord and brain to our many muscles.
small motoneurons
innervate slow-twitch muscle fibers

-are more easily excited
large motoneurons
-innervate fast-twitch muscle fibers

-not as easily excited
the size principle
-the orderly recruitment of motor units.

-weak stimuli only activates small, low threshold, slow-twitch muscle fibers

-sronger stimuli activates larger, fast-twitch muscle fibers.

-the strength of the stimulus determines what size motoneurons it will excite
-information about body movements and position.
factors that affect muscle stretch
1) rate of change of muscle length
-fcn of the weight of the load and the time over which it is applied.

-amount of energy you need to exert to keep from dropping the load
primary endings
-dynamic indicators of muscle length

-show maximum stretch in the beginning and then adapt
secondary endings
-static indicators of muscle length

-maximally sensitive to maintained length
Golgi tendon organs
respond primarily to muscle contraction.

-detect overload that threatens to tear muscles and tendons
spinal animal
-sever connection between brain and spinal cord
spinal shock
-decreased synaptic excitability in spinal cord neurons of spinal animals.

-eventually goes away.
flexion reflex
-abrupt withdrawal of stimulated limb
stretch reflex
-example of automatic control at the spinal level

1) disturbance is imposed
2) the muscle is stretched
3) the spindle fibers that are deformed inform the motoneurons
4) the motoneurons stimulate the muscle to OPPOSE the stretch (contract)
the pyramidal system
-group of cell bodies that go from cerebral cortex to the brain stem, where they cross the decussation of the medulla, and then travel down the spinal cord in the ventral corticospinal tract and lateral corticospinal tract.

-lesions of the pyramidal system deprive the patient of the ability to move individual joints and limbs.

-many of its axons originate in M1.

-right side controls the left side of the body.

-damage to M1 produces paralysis on the opposite side of the body.
primary motor cortex
-represent both movements and muscles

-disproportionate area devoted to distal muscles that are involved in most complex movements, such as the hands
nonprimary motor cortex
aids motor sequencing

-is made up of the premotor cortex and the supplementary motor cortex
supplementary motor cortex
-part of the nonprimary motor cortex

-involved in implicit movements and sequences
premotor cortex
-sequences of explicit motor learning
extrapyramidal systems
-run from forebrain-->brainstem-->spinal cord but OUTSIDE of the medulla.

-lesions exaggerate spinal reflexes.

-communicates wit hthe spin through reticolospinal and rubrospinal tracts
basal ganlia
-degeneration causes Parkinson's and Huntington's diseases.

-is made up of the:
caudate nucleus
(these two make up the striatum)
globus pallidus

is closely connected to the substantia nigra.

-helps determine the size and direction of movements

-especially important in movements influenced by memory.
endogenous oscillators
-drive repetitive movements such as walking and swimming.
central pattern generator
-the neural circuitry responsible for generating rhythmic patterns.
muscular dystrophy
-biochemical abnoramilities that lead to structural changes in muscles.

-muscles waste away.
-destroys motoneurons of the spinal cord.
flaccid paralysis
-when the spinal cord is completely severed.

-can cause excessive reflex action because there is no longer dampening input from the brain.
potential solutions to spinal cord injuries
1) stem cells
2) use of neurotrophic factors
3) transplant glial cells that support regeneration.
-the inability to cary out an act that is not due to a physical cause.
Parkinson's disease
results from lack of stimulation of the basal ganglia.

-patient shows progressive degeneration of the dopaminergic neurons of the substantia nigra.

-could be caused by exposure to toxins over time.

-is probably not inherited
-drug that reduces symptoms in parkinsons

-however, after a certain point there are too few dopamine-containing neurons left for it to work on.
Huntington's disease
-is characterized by excessive movement caused by the deterioration of the
basal ganglia.

-transmitted by a single, dominant gene.

-demonstrates the major role that inhibition plays in normal motor control.
the 4 stages of reproductive behavior
1) sexual attraction
2) appetitive behaviors
-behaviors that establish, maintain or promote sexual interaction.
-requires one or more intromissions and some copulatory stimulation.
4) post-copulatory behaviors
ex) copulatory lock, parental behaviors
refractory phase
-after one bout of copulation, the animals will not mate again for some time.

-males in many species (including humans) have an absolute refractory period after ejaculation.
Coolidge effect
-animals show a shorter refractory period when presented with a new partner.
-the female rat sex positon
tail to the side, ass up.

-only after repeated intromissions will the female rat brain release the hormones that are needed to maintain pregnancy.
activational effect
-the hormone transiently influences behavior

-no testosterone=no sex
ventromedial hypothalamus
-is crucial for lordosis

-role of VMH is to monitor steroid concentraitons and, at the right time in the ovulatory cycle, activate a multisynaptic pathway to produce the lordosis position.
medial preoptic area
-appears to integrate hormonal and sensory info to coordinate motor patterns of copulation in male rats.
-chemical signals used for communication between 2 individuals of the same species.

-are detected by the vomeronasal organ.
four response phases in human sexual cycle
1) increasing excitment
2) plateau
3) orgasm
4) resolution
human male erection
-controlled by the PGN

-PGN (in the pons) sends serotonergic fibers down the spinal cord that INHIBIT erection.

-when the forebrain is sexually aroused, it inhibits the PGN, permitting erection.

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