wk5: ND - Plasticity and Learning Flashcards

1
Q

What enables experience dependent plasticity?

A

Hebbian synaptic mechanisms

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2
Q

What Hebbian synaptic mechanisms are there? (2)

A

Long term potentiation
Long term depression

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3
Q

Explain long term potentiation

A

When an axon of cell A … excites cell B and repeatedly or persistently takes part in firing it some growth process or metabolic change takes place in one or both cells so that A’s efficiency as one of the cells firing B is increased”.

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4
Q

What type of synapse will undergo long term potentiation?

A

Synapse with vigorous pre- and post-synaptic activities

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5
Q

What type of synapse will undergo longterm depression?

A

synapse with poor or no presynaptic activity

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6
Q

Describe 3 theories about the termination of the critical period

A
  1. When axonal growth stops
  2. When synaptic transmission fully matures
  3. When activity of neuromodulators in certain cortical areas decline
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7
Q

What are the 2 classical dogmas that define plasticity beyond the critical period. What is the consequence of these dogmas?

A
  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

Note: the dogmas are wrong however

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8
Q

What evidence is there that counters currently established classicial dogmas for plasticity after the critical period?

A

Neural stem cells have been shown to divide, differentiate and even find the right targets and behave within physiological ranges
Axons and dendrites can sprout too

so the dogmas are wrong

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9
Q

What does admin of the antidepressant fluoxetine lead to in adult rats?

A

enables induction of ocular dominance shift by monocular deprivation

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10
Q

What is the role of the critical period during early development? (2)

A

Help fine tune and calibrate cortical cells
Adapt developing neurons to new environment

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11
Q

In a study by Lamberto Maffei and colleagues in Pisa, what did they find in amblyopic rats treated chronically with fluoxetine?

A

recovery in both visual acuity and C/I (contralateral/intralateral) VEP ratio. This suggests restoration of plasticity beyond critical period

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12
Q

What neat trick can you do o give yourself a bigger orgasm?

A

“Slice off your leg” - Trichur Vidyasagar

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13
Q

How can we describe sensory innervation of different parts of the body? How does this model relate to the phantom limb concept

A

Sensory homunculus. If a limb or part of body is removed, sensation may be felt if you signal an adjacent innervation area. E.g. you may feel phantom hand sensation when touching ipsilateral face

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14
Q

How are different areas of innervation in the brain represented on the sensory homunculus?

A

Representations for different parts of the brain are different. e.g Face = large resolution and large representation

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15
Q

What did pons et al. 1991 find about long term deafferentation? (1)

A

that it leads to extensive changes in cortical maps

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16
Q

What did Vilayanur Ramachandran (Sagar’s classmate, who is on youtube) conclude about phantom limbs?

A

he concluded that when the hand area loses input when amputated, adjacent areas (on homonculus) take over.

17
Q

Can patients with a phantom hand feel sensation with a mirror image? Explain?

A

If you create a mirror image of one hand, and then stroke the real hand, patients with phantom hand will feel the stroking sensation of the missing hand seen in the mirror image. Lack of inputs means the somatosensory cortex is relying on visual information alone for sensory input in the phantom hand.

18
Q

Why do normal people with 2 hands not feel a sensation from stroking a hand with a mirror imaged hand in view?

A

Because they have more inputs beyond visual information, allowing the brain to veto the visual input

19
Q

According to research from Calford, Schmid and Rosa in 1999 on an eye lesion made in an adult cat and recorded 53 days later, what did they find happened to visual receptive fields?

A

Normal eye has normal receptive field
Lesion eye acquires receptive fields outside the lesion projection zone (adjacent to it)

20
Q

According to research from Calford, Schmid and Rosa in 1999: What percentage of single neurones in the lesion projection zones (LPZ) had “ectopic” visual discharge fields displaced to normal retina in the immediate?

A

75%

21
Q

According to research from Calford, Schmid and Rosa in 1999: How does the size of ectopic discharge fields vary from the size of normal discharge fields

A

They were pretty similar/not significantly different

22
Q

According to research from Calford, Schmid and Rosa in 1999: how did the responses to stimuli presented via ectopic discharge fields compare to presentations via normal discharge fields?

A

Were generally weaker

23
Q

Describe the 3 stages of the response to a partial loss of input to the topographically-arranged representations in sensory cortex

A
  1. Immediate to hours: unmasking of new responsiveness
  2. Hours to days: new filtering of the unmasked responsiveness; synaptic plasticity
  3. Weeks to months: structural changes (local axonal sprouting, dendritic remodelling)
24
Q

Where is perceptual learning in most cases specific to? What idea does this lead to?

A

the retinal location of the stimulus, thus leading to the idea that it occurs early along the visual pathway, probably in area V1

25
Q

Is perceptual learning influenced by top-down processes? (e.g. attention)

A

yes