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162 Cards in this Set

  • Front
  • Back
what did Karl Lashley's work provide evidence for?
the distributed theory. all parts of the brain play an equal role in memory
what did Muller's work prove?
doctrine of specific nerve energies. our perceptions depend on what nerve is stimulated and not the actual stimuli.
- localized theory
what did Penfield's experiments prove?
distributed theory
- patients with specific local brain lesions produced specific behaviours
where do midget cells project to?
parvocellular layers of the LGN (layers 3,4,5,6)
where do parasol cells project to?
magnocellular layers of the LGN (layers 1,2)
where do bistratified cells project to?
koniocellular layers of LGN (in between the layers)
what LGN layers are contralateral and ipsilateral?
contra - 1,4,6
ipsi - 2,3,5
what do ON centre and OFF centre LGN cells respond to?
ON - positive contrast (centre is lighter)
OFF - negative contrast (centre is darker)
what does the magnocellular project to?
layers 4C alpha and 6 in V1
where does the parvocellular pathway project to?
4C beta, 4A and 6
what are the functions of the koniocellular pathway?
- carries the S cone signal from the small bistratified ganglion cells
- projects to the cytochrome blobs (layers 2,3 in V1)
what separates V1 and V2?
vertical meridian line
what does the golgi stain reveal?
- pyramidal cells (large cells that project out of the area
- stellate cells (interneurons)
what are the two types of stellate cells?
spiny (glutamate) and nonspiny (GABA)
what did Hubel and Wiesel discover with a cat and a crack in the slide?
V1 encodes for edges, lines and contours (it is orientationally selective)
what are the differences between simple and complex cells?
simple:
- separate on and off regions
- x like
- small RF
- in the layers of 4 and 6

complex
- same on and off regions
- y like
- large RF
- mostly outside layer 4
what are hypercomplex cells?
contains inhibitory end zones
what is hubel and Wiesel's scheme for orientational selectivity?
excitatory convergence
what did hubel and Wiesel discover about orientational columns?
similar orientations are arranged in columns that are perpendicular to the cortical surface
what are ocular dominance columns?
stripes of neurons in V1 that play a role in binocular vision
what technique can you use to demonstrate ocular dominance columns?
inject one eye with radioactive amino acids, close the other eye and then showing different orientations
what technique can show orientation columns?
injecting eye with deoxyglucose and then showing different orientations
what does cytochrome oxidase staining show?
blobs in the centre of ocular dominance columns at the supragranular layers (2,3)
what are the sources of activity in optical imaging?
blood volume, oxygenation in blood, light scattering changes from ion and water movement
what are pin wheel centres?
where all orientations converge
- first used dye but then used 2 photon imaging
- showed that orientations are completely segregated even in the very centre
where are pin wheel centres located?
over centres of ocular dominance columns. they are never at the borders
what are hypercolumns and why are they used?
they are a window the the visual world and give every possible representations of stimuli
what do blobs and interblobs tune for?
they both tune for orientation
what is the function of horizontal cells?
they link columns of cells that are similar in orientation
where do the parallel pathways first converge?
V1
do parallel pathways converge in V1?
yes
- interblob area get both M and P streams
- while blob areas get M, P and K inputs
are there mixing of parallel pathways past V1?
yes
- eg. area MT gets both colour and motion
- there are lots of communications between the dorsal and ventral streams
what is blindsight?
being to detect motion above chance even though there is a V1 lesion. due to alternative pathways to the dorsal stream (eg. konio going to MT)
what is the function of the dorsal stream and where does it project to?
for motion. projects to MT and PPC
what is the function of the ventral stream and where does it project to?
perceiving things (what). V1, V2, V4, IT
what is optic ataxia?
unable to interpret motion (spatial errors) due to a lesion in the dorsal stream
what is visual agnosia?
unable to perceive objects due to a lesion in the ventral stream.
what is visual neglect and which area of the brain is effected?
ignoring half of your visual field (normally the left field). due to a lesion in the right inferior posterior parietal cortex
what are mirror neurons?
the same neurons fire when you watch an action and doing the same action (eg. picking up a nut). basis of empathy and language
what is the pathway for pupillary contraction?
- optic nerve
- pretactal nucleus
- edinger Westphal nucleus
- ciliary ganglion
- cobtriction of pupillary sphincter
is pupil constriction sympathetic or parasympathetic?
parasympathetic
is pupil dilation sympathetic or parasympathetic?
sympathetic
what is the near triad?
set of movements that occur when we look at something close
- pupil constriction
- accommodation
- convergence
how many neurons are in the pathway of pupil dilation?
three
- down the neck
- across thorax
- up the neck and into the eye
what is Horner's syndrome?
caused by a lesion in one of the nerves for pupil dilation. it causes pupil constriction, ptosis, no sweating, dilated vessels
what drives pupil movements?
light, sense of near, arousal
what does the accessory optic system do?
an ancient system that does not project to the brain via LGN. its neurons are directionally selective and prefer large, slow movements. it is part of the optokinetic and visual-vestibular system
what are the differences between optokinetic and visual a vestibular system?
OK
- visually driven (vection)
- low frequency
- sustained response

VV
- driven by acceleration (head movements)
- high frequency
- transient response
what is the function of superior colliculus?
- smooth pursuit
- saccades?
- redirecting gaze (receives a sensory input and produces a movement)
what is the moving hill hypothesis?
- fixation cells are turned off, saccade occurs and then turned back on
- converts spatial error into temporal signal (place to rate)
how is redirecting gaze so fast?
retina projects directly to the superior colliculus and it projects directly back to the retina
do you lose gaze shift when the superior colliculus is lesioned?
no. FEF is also involved in gaze
how do we perceive objects?
- V1 detects contours and orientation
- V2 detects contours, colour and orientation
- V4 detects global shape
- IT detects shape perception
what is the pathway of motion perception?
- V1 for directional selectivity
- MT for global motion processing
- MST for complex motion processing (optic flow)
what is retinal disparity and the horopter?
horopter is a line in a depth plane. anything not in the line projects to different areas of the retina. a possible explanation for stereopsis
what are some monocular cues that can tell us about depth?
size, colour, obstruction, shading, shadows, perspectives, texture
what is binocular rivalry?
when you dissimilar objects are next to each other. you oscillate between the two, only being conscious of one at a time
what motion cues can tell you about depth?
parallax - objects at different distances have different speeds
kinetic depth - moving dots can give you an image of depth
what is inattentional blindness?
when you focus on one stimulus, you do not perceive others. eg. gorilla walking in a room
what is attentional blink?
a memory gap occurs when there is a visual surprise. you cannot process data for the next 500ms
what is exogenous attention?
bottom up
- stands out
what is endogenous attention?
top down
- hard to find
what is treismans integration theory?
when perceiving a stimulus, features are registered early (V1...?)
which area anticipates S2 in the delayed match to sample experiment?
LIP
how do LIP and MT synchronize?
LIP drives MT. creates neuronal oscillations that enhances the response to stimulus (lecture 18)
how does the fast dorsal pathway help with location selectivity?
since the dorsal pathway is faster than ventral, it will reach the MT/PPC before ventral reaches V1. MT/PPC then feedbacks to V1 to help with location selection (lecture 18)
what is the binding problem?
different information are encoded at different areas of the brain. so how then do we combine all the information together even though extra striate receptive fields have large receptive fields (they cannot encode location)
how can the binding problem be solved?
synchronicity and spotlight of attention being processed early
why do infants have poor visual acuity?
visual cortex not fully developed
- cones widely spaced and not developed
what is monocular deprivation and what is its effect in the critical period?
suturing one eye shut leads to an ocular dominance shift due to competition of inputs between contra and ipsi
what is binocular deprivation and what does it result it?
suturing both eyes shut. leads to no binocular vision, but there is still a balance of inputs between ipsi and contra
how do ocular dominance columns develop?
at birth, columns overlap each other. after the critical period they segregate and become distinct (lecture 19)
what happens to the synapses of the open eye when there is monocular deprivation?
becomes broad and dense, while the deprived eye has no synaptic connections
what time period do ocular dominance shifts occur?
critical period
what are the different types of amblyopia?
- occlusion: blocked/ptosis
- anisometropic: refractive errors
- strabismic: squinting
what is the result of amblyopia?
no binocular cells
- no stereopsis
what is the critical period?
a time period early in life where the developing nervous system adapts to the environment. a period where there is a lot of cortical changes
what is the hebbian theory?
synaptic changes depending on excitation
- LTP: strengthening of synapse when both pre and post synapses are excited
- LDP: weakening of synapse when there are no/little synaptic activity
can you induce plasticity after the critical period? give an example
yes you can. you can an induce ocular dominance shift after the critical period by using Fluoxetine (it can reverse the effects of amblyopia)
how does the cortex reorganize after deafferentiation (cutting off the dorsal roots)?
new input will be provided by adjacent areas. eg cutting off hand, the cortical area supplying the face will provide input to the hand.
what is phantom limb/pain and how do you cure it?
when you still feel your limb even though it was amputated. cure it with a mirror (eg. using the mirror so that the patient can see their phantom hand by placing the mirror next to the hand that was not amputated)
what happens in the eye (in terms of plasticity) when you lesion it?
the receptive field will get input from adjacent neurons. however, there might be inappropriate horizontal connections being applied which means a weaker response.
what is perceptual learning and where does it occur?
repetition for improved performance. probably occurs in V1
what is vection and which system produces it?
vection occurs when a large proportion of your visual field moves, and do you move in order to compensate for it. due to the optokinetic (OK) system
why do we have vection? in evolutionary terms
we have evolved in such a way that when our visual field moves, it means that we are moving
what are the 3 sources that help us to orientate?
visual, proprioception (joints and muscle senses), vestibular system
what are the otilith organs and what do they sense?
utricle and saccule. detects linear acceleration
- utricle = coronal/horizontal plane
- saccule = sagittal/vertical plane
how do the otilith organs sense acceleration?
calcium carbonate crystals bend hair cells/kinocilium.
- towards K causes depolarization
- away from K causes hyperpolarization
- action potentials produced during hyperpolarization
what are semicircular canals and how do they work?
3 perpendicular canals that sense angular accelerations (head rotation). the capulla inside the ampulla lags behind the endolymph fluid when the head rotates. the kinocilium and hair cells respond as the capulla lags behind.
what is the vestibular ocular reflex?
when your eye moves in the opposite direction of head rotation (eye remains fixated)
does anaesthetics alter the response of ERG waves?
yes. use wireless for more accurate results
what is the function of the blood brain/retinal barriers?
to regulate substances from the blood stream
what are the two blood neural barriers and how do they work?
mechanical - formed by tight junctions (occludin, JAM, claudin) to prevent large substances

metabolic - formed by GLUT1 and GLUT3 to pump in specific substrates
where are the neural barriers in the brain and retina?
brain - cerebral vasculature endothelium

retina - RPE in outer and endothelium in inner (note: no barrier at PR layer because they are very metabolically active)
what does fluorescin angiography show?
the dye shows how substances are confined to the blood vessels only. they do not leak out unless there is a breakdown in the barriers
does the eye have similar blood pressure regulation as the brain and what does it mean?
yes they do. it means that BP of the brain can be examined via the eye
how is diabetes examined via the eye?
loss of pericytes, lack of barrier, etc
how are hypertension and stroke examined?
looking at the arteries and veins in the retina
- quantifying a ratio between the two
how is multiple sclerosis examined by the eye?
barrier breakdown, GC and inner plexiform layer thinning
how is Alzheimer's diagnosed via the eye?
AB plaques, GC layer thinning, vasculature changes
what is Laughlin's rule?
efficiency is maximised between a cell's stimulus response relationship and the entire distribution of input signals
what are the regions of the light adaptation curve?
- dark light region: absolute threshold region
- Rose-deVries region: Intensity proportional to sqrt background intensity
- Weber's region: intensity proportional to background intensity
what are the two explanations for Rose-DeVries and what are their differences?
classical - intensity increases in order to compensate for the increase in background noise (no adaptation)

alternative - intensity increases in order to compensate for the reduced gain (adaptation)
what is gain?
difference between stimulus and response...?
what is adaptation pooling and why do we need it?
adaptation for low lights occur after the cones/rods at the level of GC. adaptation is delayed so that signals are converged for a more reliable signal. (note: adaptation for high levels of light occur at the photoreceptor because there is already enough info)
what are the properties of the S2 region for dark adaptation?
- it represents the exponential decay of opsin (rate: 0.24log]
- occurs at all levels of bleach
- for every 1% of bleach pigment it takes 7 minutes (occurs when bleach exceeds 10%)
- it is rate limited
what are the properties of region S3 in dark adaptation?
- seen in bleaches greater than 20%
- Rate of 0.06log
how are cones arranged in the retina?
S - sparse
L and M ratio highly variable
they are all in random arrangements
what is our spatial resolution limit?
40-60 degrees eccentrically
what limits our contrast in central vision? and what evidence is there?
the optics limits our contrast sensitivity in central vision. interferometry greater than CSF
what limits our contrast sensitivity in the peripheral?
it is not the optics since interferometry = CSF in the periphery. most likely the midget ganglion cells since they pool information from the periphery (they have small RF size and cover all eccentricities)
how far into the periphery is there half the cones compared to the centre?
0.2 degrees eccentrically
how do we resolve fine detail?
detector/photoreceptors are very small and the arrangement of detectors/photoreceptors is very fine. this allows for a high sampling frequency
what is aliasing and how does it occur?
occurs during under sampling (when sampling is less than twice of the signal frequency). it produces a signal that is lower in frequency and with a different orientation than the original
what is the Nyquist limit?
f = n/2 : predicts aliasing
how does the eye help prevent aliasing?
blurring of the eye's optics
why are S cones so sparse?
the S wave is blurred by the optics due to chromatic aberration. so s cones being sparse is adequate enough to capture an image
what resolves resolution in the periphery and what does it mean in terms of glaucoma diagnosis?
density ganglion cells. this means that measuring resolution performances can determine the severity of glaucoma
what is oculomotor procrastination?
the time it takes for higher level processes to decide the suitability of a target
- it reflects decision making time
what is saccadic latency?
the delay between a visual target and the saccade
how is the LATER graph formed?
raw to reciprocal to cumulative to probablility
how is a response generated in decision making?
- a stimulus
- decision signal rises at a constant rate from S0
- one it reaches the threshold (St) a response is generated
what affects the decision signal?
- expectation: S0 increases
- rate of information
- urgency : St decreases
how does urgency effect decision making?
there is less time for information to accumulate. so evidence will be driven by the initial information
in the LATER model, what happens when you increase probability?
decrease the latency time (S0 decreases)
what is gratitious randomization?
your response to a stimulus is not determined by input
- random behaviour
describe the random walk model
accumulation of noisy signal to produce a response (like flipping a bias coin)
- the rate of rise is random, unlike the LATER model
what is the two stage model in decision making?
1. random walk (detection)
2. LATER (decision)
which decision making model dominates at low contrast?
random walk
which decision making model dominates at high contrast?
LATER
what evidence are there for the two stage model of decision making?
- probability and contrast add linearly (they are independent)
- global parameters (urgency,expectation) only effects 2nd stage
- the slopes of latency at 50% are horizontal. they do not cover the whole range, so both models are needed
- neurophys: oddball search.
which cranial nerve supplies the vestibular system?
CN8 - vestibulocochlear
where do the cranial nerves for the eye muscles originate and which dessucates?
oculomotor CN3- midbrain
trochlear CN4- midbrain and dessucates
abducens CN6- pons
how are saccades generated?
1. burst of innervation from excitatory burst neurons
2. tonic innervation at abducens
3. burst and tonic combine at abducens to form a pulse-step innervation
what is the tract that joins the abducens to the oculomotor for conjugate eye movements?
MLF - medial longitudinal fasciculus
which area commands for intentional saccades?
FEF
which area produces reflexive saccades?
PPC
which area produces inhibitory reflexive saccades?
DLPFC
which eye movementsndoes the superior colliculus generate?
smooth pursuit and saccades?
what types of stimuli is for smooth pursuit?
real or perceived
what clinical use for eye movements can be used to indicate pathology?
pathology when you smooth pursuit in one direction and saccade the other way
what is ocular myasthenia and how can it be treated?
an autoimmune disease that attacks the ACH receptors. the post synapse is also distorted such that cholinesterases are close to the surface.
treat with tensoline or ice
what is internuclear opthalmoplegia (INO) and what does it cause?
occurs when there is damage to the MLF. contra eye cannot adduct when the ipsi adducts. does not effect convergence unless the lesion is very big
what is marcus-gunn jaw winking and how is it caused?
a congenital synkinesis (miswiring of nerves)
- trigeminal innervates the levator
what is Duane's retraction syndrome?
occurs when there is no innervation of the lateral rectus. the oculomotor nerve then sends out a branch to the LR to innervate it. this causes co-contraction of MR and LR. so the eye adducts, it also retracts
what happens in 3rd nerve palsy? (abberation regeneration)
- you are unable to adduct, elevate or depress
- ptosis
- pupil dilation
- after some time, the nerve will try to regenerate but it may go the wrong way. eg eyelids elevaing when you look down, or eyes going in opposite directions
what is nystagmus?
a condition where your eyes move involuntary
is congenital nystagmus commonly symptomatic?
no. they adapt to it during development
what happens in social phobia in terms of eye movements?
avoidance of eyes
what is ventral simultanagnosia?
you trace objects correctly, but you cannot perceive it
what is the main problem with saccades and how does the brain solve it?
rapid motion of the eye will cause a blur. solved with saccadic suppression
what is saccadic suppression?
when the brain shuts itself down (but not completely) just before and during a saccade
which areas are effected by saccadic suppression?
eye, LGN, V1, SC, PPC, IT
what occurs in post saccadic enhancement?
enhanced response, reduced delay
what is time compression?
we perceive time to be short before and during a saccade. due to the first response being normal and the second being faster
what is chronostasis and how does it occur?
time expansion: we perceive time to be longer after a saccade.
due to a short first response and normal second response
what is time inversion and how does it occur?
we perceive time to be backwards just before a saccade. due to the 2nd response reaching the brain first due to post saccadic enhancement
where are the common places for the bionic eye to be placed?
epi-retinal: between GC layer and vitreous
supra-choroidal: between choroid and sclera
sub-retinal: in the PR layer
what is the advantages and disadvantages of supra-choroidal?
it is easily fixated.
needs a lot of current since it is further away from the BC
what cells are targeted by the bionic eye?
bipolar cells
what does stimulation of the bionic eye produce?
phosphene vision (spots of light)
what are the scientific challenges of the bionic eye?
1. it needs to stimulate a suitable current
2. charge needs to be localized
3. needs to be long lasting