L13: Central Visual Processing II (Visual Development and Neural Plasticity) Flashcards

1
Q

Define synaptic plasticity

A

ability of a synapse btw two neurons to change in strength or effectiveness

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2
Q

Explain the OD scale (1-7)

A

ocular dominance scale
1 = a cell that is completely dominated by contralateral eye input
4 = a binocular cell equally driven by either eye
7 = a cell that is dominated completely by ipsilateral eye

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3
Q

Explain the normal distribution of cells in terms of OD scale in the visual cortex.

A

nearly equal numbers of cells driven by each eye

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4
Q

Explain what happens in monocular deprivation soon after birth when an eyelid is sutured soon after birth and remains closed for 6 months.

A

After opening the eyelid, recordings in V1 show that nearly all cells are driven by the eye that wasn’t sutured close (e.g. nearly all cells had OD = 1 or 7). This was a permanent change due to changes in V1 itself, not in the retina, LGN or option radiations.

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5
Q

What is amblyopia?

A

Amblyopia is a type of central (cortical) loss in vision without apparent abnormality in the eye.

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6
Q

Why is it that in monocular deprived eyes the deprived OD column bands are much thinner while the non-deprived eye bands are much wider than normal?

A

Due to an interplay btw axonal growth, activity-dependent synaptic competition and the differential pruning or strengthening of connections

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7
Q

Will monocular deprivation lead to abnormal OD development if performed at any time of life and development?

A

No, Hubel and Wiesel discovered that abnormal OD development only occurred if performed btw birth and about 6-8 years in a human child. This time window is called the critical period.

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8
Q

What is the critical period?

A

The critical period is when monocular deprivation will actually cause abnormal OD development because this is when connections are highly susceptible to stimulus input.

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9
Q

Can effects of monocular deprivation be reversed?

A

Yes, it can be partially reversed if the deprived eye (e.g sutured eye) is unsutured/opened & the normal eye is now sutured. during the critical period.

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10
Q

What happens when there’s binocular deprivation during critical period?

A

It seems to lengthen the critical perioid. And if extended, the binocular deprivation leads to a paucity of binocularly driven cells and strong OD column bands with borders that are abnormally sharp

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11
Q

What does the expt on binocular deprivation in which the OD column bands have abnormally sharp borders say about what’s going in?

A

It shows that effects of monocular deprivation are not due to disuse rather due to active competition because if it were due to disuse then in the binocular deprivation expt, there should be no cells that can see.

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12
Q

Compare and contrast strabismus and amblyopia

A

Strabismus is a periperhal disorder while amblyopia is a central disorder. Strabismus involves the EOM, causing a misalignment of the 2 eyes, preventing proper binocular vision.

Amblyopia is a central disorder when there’s nothing wrong with the eye but is due to an imbalance or lack of visual coordination btw the 2 eyes during development, leading to poor vision or acuity in one eye.

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13
Q

What other conditions can lead to amblyopia?

A
  • Strabismus in young can lead to amblyopia
  • refractive errors
  • cataracts
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14
Q

“Patch the good eye” therapy

A

Amblyopia in the young should be fixed before the end of the critical period to cover the good eye. HOwever, this can lead to poor stereopsis (binocular depth vision)

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15
Q

What does normal visual development require (2 components)?

A

both a match in strength of input from each eye AND a coordination of inputs (synchronous inputs = seeing the same thing at the same time with both eyes)

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16
Q

What are some outcomes of strabismus?

A
  • alternation of 2 strong eyes

- amblyopia (1 weak eye)

17
Q

State Hebb’s hypothesis

A

“Cells that fire together wire together” -any two cells or systems of cells that are repeatedly active at the same time will tend to become associated so that activity in one facilitates activity in the other

18
Q

Explain the competition that’s going on in monocular deprivation and binocular deprivation

A

In monocular deprivation, the deprived eye cannot generate much synchronized cortical input, and thus loses out in the competition for V1 territory. In binocular deprivation, neither eye has a competitive advantage, so the OD columns are closer to normal just more in the extreme ends

19
Q

What happens when you inject TTX in the eyes?

A

It will silence retinal output by blocking presynaptic activity, which will suppress the effects of MD since the effects of MD depend upon activity.

20
Q

What happens when you apply GABA in the cortex?

A

It will silence the cortical cells by blocking post-synaptic activity in the cortex, suppresses the effects of MD since the effects of MD depend on activity

21
Q

What happens when you electrically stimulate the optic nerves after TTX injection in the eyes synchronous or asynchronous?

A

Electro stimulation asynchronous by eye leads to OD columns, but if electo stim is applied synchronously to the 2 optic nerves, no segregated OD columns form.

22
Q

Explain the role of NMDA in ocular dominance plasticity

A

It is a critical component in ocular dominance plasticity.
Evidence:
1-NMDA receptor antagonists reduce OD plasticity and the refinement of receptive-field properties
2-overall [NMDA receptors] in the visual cortex peaks with the critical period for OD plasticity
3-NMDA contribution to the visual cortex drops in layers IV, V, VI as ocular dominance columns segregate
4-rearing in the dark postpones these changes, as it does OD segregation and other events during critical period

23
Q

How did the 3-eye frog expt show that synaptic competition leads to functional segregation?

A

A frog’s optic tecta is normally innervated by one optic nerve. When you implant another eye, it will grow a 2nd optic nerve to innervate the optic tecta. This 2nd optic nerve sets up a synpatic competition that yields an OD column-like segregation in the tectum that wasn’t there before.

24
Q

Explain the “covering-up” that is associated with the blind spot

A

The filling-in of the blind spot implies a constant, active cortical process/mechanism for “covering up” the lack of input activity.

25
Q

What is going on with the phantom limb?

A

the limb is no longer there, but it is felt due to cortical reorganization of the somatotopic maps in somatosensory cortex. The sensory cortex craves input an will adjust its synaptic weights, grow new connections and expand its territory in order to find and obtain a sufficient amt of input activity, even from phantom limb.

26
Q

List 4 examples of adult cortical plasticity

A

1 - recovery from brain injury or stroke
2 - rapid fill-in of the cortical representation after a retinal lesion, followed by a longer-term axonal growth
3 - analogous cortical reorganization of somatotopic maps under conditions of digit re-afferentation (following digit amputation) or digit “melding,” or in limb amputees
4 - phantom limb sensations/pain that may be explained by cortical reorganization of the somatotopic maps in somatosensory cortex.

27
Q

Initially by depriving the sensory cortex of input (either using laser lesioning in the retina or digit amputation of the hand), they found that the sensory cortex was SILENT in the region deprived of input. But what eventually happens?

A

But after time, that cortical region became active again, resulting in a shift in the topographic maps because the input deprived cortex had stolen from adjacent cortex using the same mech of competition and plasticity. (explains the phantom limb phenomenon)

28
Q

Children with congenital cataract and undergo surgery too late (10 yrs old), will be functionally blind in affected eye. But if surgery occurs earlier in life, no such defect. Explain.

A

This indicates that vision continues to develop from birth to up until a certain age. In these situations, those affected children have a form of eye disorder known as amblyopia in which