Week 2 - Visual Development and Neural Plasticity

Question 1

what is synaptic plasticity?

Answer 1

ability of a synapse between 2 neurons to change in strength or effectiveness
-visual/sensory experience VS genetic/intrinsic programming VS intrinsic development cues and rules

Question 2

what are interrelated processes in vision?

Answer 2

neural development, plasticity, learning, reorganization, and recovery
-all share common mechanisms

Question 3

what did visual deprivation experiments show?

Answer 3

there’s a role of visual experience and synaptic competition in normal visual development

Question 4

what is the “critical period”?

Answer 4

a time window in development when connections are highly susceptible to stimulus input
-a few days of deprivation can permanently alter development of OD columns

Question 5

what is synaptic competition closely linked to?

Answer 5

Hebb’s hypothesis

“cells that fire together, wire together”

Question 6

what is the first site of binocular interaction int he visual system?

Answer 6

primary visual cortex

Question 7

what does intravitreal injection of 3H-proline show in adult VS fetus/neonate?

Answer 7

3H-proline is a trans-synaptic tracer

• reveals pattern of ocular dominance columns (after autoradiographic processing); transported back to thalamus, jumps synapse, and causes pattern in layer 4 of V1
• in adult, will show layering pattern
• in fetus/neonate, no ocular dominance columns (continuous color)

Question 8

what do 3H-proline studies imply?

Answer 8

when the LGN afferents first invade the cortex, they come in unsegregated according to eye of origin (LGN layer of origin)

Question 9

what is the difference between having congenital cataracts and adult cataracts?

Answer 9

children who underwent surgery too late (10 years old) were functionally blind in that eye, but the same surgery in adults would yield good vision (form of amblyopia)

Question 10

what is the OD scale? what is it in normal adults?

Answer 10

recording from single cells in V1, classifying each cell’s response to visual stimuli from 1 to 7

• 1 is completely dominated by contralateral eye
• 7 is completely dominated by ipsilateral eye
• 4 is equally bilateral
• in adults, there are equal numbers of cells drien by each eye

Question 11

what did the monocular deprivation studies show? how did they come about?

Answer 11

the “good eye” would take over territory normally occupied by other (occluded) eye, creating skewed historgram

• due to changes in V1 itself, not retina, eye, LGN, or optic radiations
• interplay between axonal growth, activity-dependent synaptic competition, and differential pruning/strengthening of connections

Question 12

what is amblyopia? what can it be caused by?

Answer 12

central (cortical) disorder from imbalance or lack of visual coordination between the 2 eyes during development

• leads to poor vision acuity in one eye, compared to other “strong” eye, w/o apparent abnormality in the eye
• can be caused by strabismus, refractive errors, and cataracts

Question 13

how did monocular deprivation show critical period?

Answer 13

• if 2 wk old covered for 18 mo, or 10 wk old covered for 4 mo, would have very unequal skewing
• if i yr old covered for 1 yr, still skewed, but there are some connections on deprived side
• if 6 yr old covered for 1.5 yrs, it has more normal distribution, but almost no binocular vision

Question 14

what does “reverse suturing” mean and do?

Answer 14

original suture is opened and non-sutured eye is now sutured, during the critical period
-forces use of weakened eye, and it can partially regain lost cortical territory (back in competition)

Question 15

what does binocular deprivation at birth or during critical period do?

Answer 15

lengthens critical period, leading to paucity of binocularly driven cells (but no 4, although still abnormally sharp monocular)
-shows that tissue is not “disused”, but “competitive”

Question 16

what is strabismus?

Answer 16

peripheral disorder, involving extraocular muscles, causing misalignment of 2 eyes, preventing proper binocular vision

• if occurs in young, often leads to amblyopia
• AKA heterotropia, squint, deviated eye, cross-eye

Question 17

what does normal visual development require?

Answer 17

both match in strength of input from each eye, and coordination of inputs (synchronous input, seeing same thing at same time)

Question 18

what is stereopsis and what can make it poor?

Answer 18

poor depth vision can be caused by binocular deprivation at birth, or strabismus (alternation or amblyopia) b/c there was never a chance for good coordinated binocular input

Question 19

how can one prevent double vision?

Answer 19

diplopia can be avoided by suppression or alternation

Question 20

what is Hebb’s hypothesis?

Answer 20

any 2 cells or systems of cells that are repeatedly active at the same time become “associated” so activity in one helps activity in the other

• when one cell repeatedly assists in firing another, the axon of the first cell develops or enlarges synaptic knobs in contact with soma of second cell
• contribute to neural development and learning
• locus of Hebbian interactions is at the ionotropic NMDA receptor

Question 21

what would happen if cell A (left eye) and cell B (right eye) both synapse on cell C, but there’s higher synchronized activity between B and C?

Answer 21

if there’s more firing between B and C, that means the synapses between B and C will strengthen at expense of A and C

Question 22

how can Hebbian competition be tested?

Answer 22

1. binocular deprivation (neither eye has competitive advantage, so OD columns are normal)
2. intravitreal injections of TTX (silence retinal output by blocking presynaptic acctivity, suppressing effects of MD)
3. GABA application on cortex (silences cortical cells by blocking postsynaptic activity, suppressing MD)
4. artificial electrical stimulation after TTX (if asynchronous, creates OD columns, but if synchronous, no segregated OD form)

Question 23

what is the role of NMDA in ocular dominance plasticity?

Answer 23

1. antagonists to NMDA receptors reduce ocular dominance plasticity and refinement of receptive-field properties
2. overall concentration of NMDA receptors in visual cortex peaks w/ critical period for ocular dominance plasticity
3. NMDA contribution to visual response drops in layers IV, V, and VI as ocular dominance columns segregate
4. rearing in dark postpones changes as it does ocular dominance segregation and other critical period events
   * in short, NMDA receptors fulfill 3 of the criteria for a substance that is higher in young animals than in adults, and is also in plasticity pathway, so is a critical component

Question 24

what do the 3-eyed frog experiments show?

Answer 24

activity-based competition leads to segregation even in a system that normally lacks segregation
-normal, 2-eyed frogs don’t show segregation (they have complete crossing)

Question 25

how is phantom limb explained?

Answer 25

sensory cortex will adjust its synaptic weights and grow new connections to expand territory in order to find and obtain a sufficient amount of input activity, even from functionally inappropriate sources

• so, if the arm is amputated, the thumb/hand area of the cortex will spread out to face or trunk (via homonculus cortex)
• if someone touches the face or trunk, it will be like someone is touching the hand that is no longer there