Plasticity and Simple Motor Learning Flashcards

1
Q

What does delay eye blink conditioning involve?

A

pairing a conditioned stimulus with an unconditioned stimulus which naturally causes an unconditioned response

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2
Q

Describe eye blink conditioning before and after training

A
  • before - the US causes the UR and the CS causes no response
  • after - the CS causes the CR before the US is delivered
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3
Q

What does eye blink conditioning involve?

A

repeatedly pairing the CS with the US and over time, the subject learns to associate the two stimuli

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4
Q

What are the 3 key features of delay eye blink conditioning?

A
  • time (CS is presented first and remains on until the US is presented)
  • learning the association
  • role of the cerebellum
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5
Q

What are the 3 phases of delay eye blink conditioning?

A
  1. acquisition – subject learns to associate a CS with a US; over time, the CS alone evokes a CR (anticipatory eyeblink before the US is presented)
  2. extinction – CS is presented without the US; over time, the subject learns that the CS is no longer predictive of the US and the CR decreases in magnitude and frequency, which represents the subject’s unlearning or inhibition of the previously learned association (eventually no blinking is seen in response to CS as the association is weakened/suppressed)
  3. reacquisition – CS is once again paired with US and the subject begins to relearn the association between the two; typically happens more quickly than the initial acquisition since the subject has a memory of the previous learning
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6
Q

What does the rapid relearning in reacquisition indicate?

A

the initial association wasn’t entirely erased but was inhibited or suppressed during extinction

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7
Q

What cells does the cerebellar cortex contain?

A

Purkinje, granule and stellate cells

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8
Q

What are Purkinje cells?

A

inhibitory neurons with their cell bodies in the cerebellar cortex

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9
Q

What does each Purkinje cell receive?

A

monosynaptic excitatory input from a single climbing fibre and 100,000 granule cells via parallel fibres

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10
Q

What does each granule cell receive?

A

excitatory input from ~4 mossy fibres

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11
Q

What does climbing fibre stimulation evoke?

A

complex spikes in Purkinje cells which help with motor learning and correcting errors during movement

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12
Q

What does mossy fibre stimulation evoke?

A

simple spikes which help with ongoing motor control and fine-tuning

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13
Q

What is the role of the cerebellum in delayed eye blink conditioning?

A

it integrates sensory information from the CS and US, leading to the CR after training

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14
Q

What does LTD do at the granule-Purkinje synapse?

A

weaken the inhibition on the deep cerebellar nuclei, which facilitates the condition of the CR

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15
Q

When does LTD occur at the granule-Purkinje synapse?

A

when the granule cells and climbing fibres fire together

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16
Q

When does LTP occur at the granule-Purkinje synapse?

A

when granule cells fire alone without climbing fire activity (deep cerebellar nuclei inhibit climbing fibres)

17
Q

What is the Marr-Albus hypothesis?

A

a computational model that proposes that the cerebellum controls movements entirely by itself

18
Q

What is Kamin blocking?

A

failure to learn an association between a new stimulus and a US when the new stimulus is presented alongside a CS that already predicts the US

19
Q

What happens when the CS is presented without a US without deep cerebellar nuclei control?

A

granule cell activity coincides with climbing fibre activity, leading to LTD at the granule-Purkinje synapse, which weakens Purkinje cell inhibition on the deep cerebellar nuclei which prevents extinction i.e. CR persists

20
Q

What happens when the CS is presented without a US with deep cerebellar nuclei control?

A

climbing fibres are inhibited which allows granule cells to induce LTP at the granule-Purkinje synapse, leading to increased Purkinje cell inhibition on the deep cerebellar nuclei which reduces the CR i.e. extinction persists

21
Q

What is prediction error?

A

discrepancy between what is expected and what actually happens

22
Q

What does the Rescorla-Wagner model explain?

A

how the strength of associations between a CS and US change over time through learning

23
Q

What does the Rescorla-Wagner model assume?

A

there is a limit to the strength of the association; initially the association is weak/non-existent, but with repeated pairings, the association grows until it reaches a maximum strength (asymptote)

24
Q

When will learning occur with delay eye blink conditioning?

A

when the outcome (US) differs from what is expected

25
Q

What are limitations of the Rescorla-Wagner model?

A
  • does not account for latent inhibition; when a CS is presented without a US for a while before conditioning, it becomes harder to learn the CS-US association
  • does not handle contextual effects well, where the environment plays a role in conditioning
  • assumes a linear relationship between learning and prediction error
26
Q

How do climbing fibres encode positive and negative prediction errors?

A
  • before learning, climbing fibres are relatively inactive because there is no expected outcome
  • during acquisition, they signal a positive prediction error (unexpected US) and Purkinje cells adjust their firing through LTD, allowing the CR to develop
  • during extinction, when the CS is presented without the US, they encode a negative prediction error, leading to a weakening of the learned response
  • after training, the CS pauses Purkinje cell activity because LTD weakens the excitatory input from granule cells, allowing the deep cerebellar nuclei to trigger the CR
27
Q

What 2 things do complex spikes in Purkinje cells show?

A
  • positive prediction error to US before training i.e. outcome is better than expected, enhanced learning
  • negative prediction error to CS alone after training i.e. outcome is worse than expected, weakened learning
28
Q

When do dopamine neurons show phasic firing?

A

when there is a surprising or unexpected event; firing rate is increased in response to a positive prediction error and decreased in response to a negative prediction error

29
Q

What is ocular dominance plasticity?

A

the brain’s ability to change the strength of input from each eye to the visual cortex

30
Q

Which properties first arise in V1?

A
  • orientation selectivity
  • binocular responses
31
Q

What is the result of closing an eye during the critical period?

A
  • V1 responses are shifted to favour the open eye
  • ocular dominance columns of the closed eye are shrunk
  • ocular dominance columns of the open eye are expanded