visual development Flashcards

1
Q

How did they find out that baby’s vision isn’t developed?

A

Through usign visual evoked potentails and using gratings and analysing results to reconstruct image.

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2
Q

What leads to ocular dominance shift?

A

monoocular deprivation

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3
Q

Why babies can’t see?

A

Not bcse optics.
While rod-dominated peripheral retina of the new-
born appears normal, the all-cone fovea contains
widely spaced and poorly developed cones.
* Visual cortex is not fully developed.

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4
Q

what are the underpinning hebian mechanisms resulting in ocular dominace shift?

A

LTP: open eye input. LTD:closed eye input and Inhibitory synapses
may become stronger
and/or alter network
properties to enable
LTD

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5
Q

what happens when you suture both eyes?

A

Few binocualr cells develop. Although receptive fields are not imapcted.

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6
Q

why are there uniform distribution in first 2 weeks?

A

LGN afferents terminating in layer IV of
striate cortex have markedly
overlapping arbors

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7
Q

process of marking ocular dominance coloumns?

A

you inject the radioactive amino acid that gets taken
up by the retinal ganglion cells take it up to
the the LGN nucleus.
It goes across the synapse, get taken up by the
postsynaptic cells and the postsynaptic cells.
Then take it right up to the primary visual cortex.

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8
Q

When are ocular domiance columns visible?

A

Distinct ocular dominance patterns are
evident within about 6 weeks in layer IV
(cat and monkey

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9
Q

how do Geniculocortical axon arbors in layer IV in normal cats
and after monocular deprivation present?

A

In young: terminal wide, expand over a large region.
In mature: condensed compact
open monoocualr deprivation: terminals broader
closed: thinly sparse.

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10
Q

ocular dominance shift: how and why

A
  1. There is competition between the
    geniculocortical inputs related to the two eyes for
    cortical space.
  2. In the absence of inputs (visual experience)
    originating in one eye, the inputs related to the
    other eye takes over the cortical space.
  3. Note that it is form vision, not simple
    diffuse light, that is essential to establish
    normal connectivity.
  4. There are very few changes earlier along
    the visual pathway - in the retina and LGN,
    except some shrinkage of cells in the
    deprived LGN laminae.
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11
Q

ocular domiance shift: when does it occur?

A

During critical period of close to 1 week in first few weeks of life.

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12
Q

can you reverse ocular dominance shift during critical period?

A

yes. even for 14 days reversal.

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13
Q

why critical periods don’t last?

A

Theories about termination of Critical Period:
1. When axonal growth stops… when they lose their
ability to change terminal length.
2. When synaptic transmission has fully matured…from
changes in post-synaptic receptors (glutamate,
NMDA, GABAergic inhibition, etc.)
3. When activity of neuromodulators (norepinephrine,
acetylcholine, etc.) in certain cortical areas decline.

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14
Q

critical periods across vision?

A

Bionocular vision has varying critical periods across species. In humans 3-4 years. Different visual
functions have
different critical
periods

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15
Q

Is critical period restricted to vision?

A
  1. Occurs in other sensory systems too, for example the
    auditory system of barn owls (Knudsen, 1999; DeBello
    et al., 2001) and cats
    during early life.
  2. There is also competition between different sensory
    modalities (vision, touch and hearing), similar to
    competition between two eyes (Vidyasagar, Nature,1978;
    Rauschecker, Trends in Neurosci.,1995): e.g., there is a greater
    neuronal pool devoted to auditory and somatosensory processing in a visually deprived animal.
  3. Imprinting: birds can be shown to imprint on any object exposed
    to them immediately after birth (Konrad Lorenz: King Solomon’s
    Ring)
  4. Language development: E.g., in children rescued from wolves
    or from total social isolation?
    ! Why is there a critical period?
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16
Q

CLASSICAL FRAMEWORK OF CRITICAL PERIODS

A

For sensory systems to develop fully, normal visual
experience is necessary.
* There is a ‘critical period’ (CP) during early life, when
developing visual system is susceptible for environmental
influences.
* Changes specific to CP involve axonal and dendritic
sprouting, experience-dependent competition, pruning of
axons, neuromodulators, etc.
* After the critical period, it is not possible to induce
changes in early sensory areas.
Classical framework

17
Q

beyond critical period, plasticity after adulthood

A

Not much is goin gto change.
1. Nerve cells in the adult do not divide
2. There is no significant growth of nerve fibres.
Consequence: Only changes in synaptic strength (i.e., Hebb synapse)
can mediate plasticity….. for learning and memory, recovery
after injury, etc.

18
Q

Can plasticity be restored and how?

A

Neural stem cells have been shown to divide, differentiate and
even find the right targets and behave within normal
physiological ranges!
* Axons and dendrites can sprout!
Plasticity beyond critical period

19
Q

what is activated during reading?

A

Visual word form area.

20
Q

what else can activate the wisual word form area?

A

Braille reading in the blind also activates the same ‘Visual
Word Form area (VWFA) as in the normally sighted.

21
Q

How is cross modality shown in the blind?

A
  1. A small number of both early-blind and late-blind
    people can teach themselves to echolocate using the
    reflections of the sound they produce (similar to bats!).
  2. In both, activation can be shown to occur in the
    calcarine (visual) cortex.
  3. In both, activation was seen in middle temporal and
    nearby cortical regions when they listened to echoes
    reflected from moving targets.
    Blind man using tongue clicks and echolocation to “see”
    the world
    Thaler et al., PLosONE., (2011)
22
Q

How can plasticity be restored after critical period?

A

Administration of
antidepressant, fluoxetine
(selective serotonin
reuptake inhibitor) to adult
rats enables induction of
ocular dominance shift by
monocular deprivation.

Amblyopic rats
chronically treated with
fluoxetine showed recovery
in both visual acuity
(above left) and in the C/I
VEP ratio (below left).
Restoring plasticity beyond critical period
(Lamberto Maffei & colleagues in Pisa)

23
Q

What are the pharmacological mechanisms of adult platicity?

A

Reduction in
inhibition +
persistent changes
at excitatory
synapses +
modulation by
acetylcholine via
astrocytes

24
Q

What is the evidence of exercise in restoring plasticity?

A

Mice, growing with enriched environment (with access to
running wheels), show life-long ocular dominance
plasticity. as well as ones experiencing stroke.

25
Q
A