skill acquisiton Flashcards

1
Q

what is skill aquisition

A

ability to reliably deliver accurate execution

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2
Q

What occurs during skill aquisition

A

there is a speed-accuracy trade-off and slow learning
there are cellular changes ie neuroplasticity
and can be system level changes

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3
Q

what are system levels for skill acquisition

A

move from cortical to sub-cortical
automatisation
decreased cognitive effect

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4
Q

what are the four mechanisms of motor learning

A

Instructive
reinforcement
use-dependent
sensorimotor adaptation

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5
Q

what is instructive motor learning?

A

strategy based, explicit
primary driver = performance-based external feedback
primary neural substrate involved is prefrontal cortex
cognitive load = high

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6
Q

what is reinforcement motor learning

A

Reward-based
Primary driver: outcome-based external feedback
primary neural substrate involved: basal ganglia
Medium cognitive load

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7
Q

What is use-dependent cognitive learning

A

Repetition based
Primary driver: task-specific massed practice
Primary neural substrate involved: motor cortex, spinal cortex
Medium cognitive load

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8
Q

What is sensorimotor adaptation

A

recalibration, implicit
Primary driver: sensorimotor prediction errors
Primary neural substrate: cerebellum
Low cognitive load

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9
Q

what is the process of long-term potentiation

A

Voltage-gated NMDA receptors in membrane at a new synapse site
Ca2+ influxes only when there is coactivation of pre and post-synaptic membranes
Ca”+ influx stimulates insertion of non-voltage gated AMPA receptors into membrane

AMPA receptors can’t figure out useful connection till both fire at same time so initially connection is weak

There is a resultant increase in post-synaptic neuron receptors
Originally nerve 1 cant make nerve 2 work but after time body realises possible useful connection and AMPA receptors easier for nerve to carry signal

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10
Q

what is long-term potentiation

A

a cellular mechanism of memory formationin the brain
persistent strengthening of synpases based on recent patterns of acivity

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11
Q

what is the process of long term depression?

A

if connection isn’t being used or is unhelpful the connection can be removed
this stops nerve 1 directly impacting on nerve 2
opposite process to potentiation
decrease post-synaptic Ca2+ results in reduction of AMPA receptor initially
followed by deletion of synapses if continued failure to coactivate
may completely lose synapse

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12
Q

what are the 10 principles of experience-dependent plasticity

A

use it or lose it
use it and improve it
specificity
repetition matters
intensity matters
time matters
salience matters
age matters
transference
interference

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13
Q

what is the use it or lost it principle

A

failure to drive specific brain functions can lead to functional degradation

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14
Q

what is the use it and improve it principle

A

training that drives a specific brain function can lead to an enhancement of that function

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15
Q

what is the specificity principle

A

nature of the training experience dictates the nature of the plasticity

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16
Q

what is the repetition matters principle?

A

induction of plasticity requires sufficient repetition

17
Q

what is the intensity matters principle

A

induction of plasticity requires sufficient training intensity

18
Q

what is the time matters principle

A

different forms of plasticity occur at different times during training

19
Q

what is the salience prinicple

A

the training experience must be suffiently salient to induce plasticity

20
Q

what is the age matters principle

A

training-induced plasticity occurs more readily in younger brains

21
Q

what is the transference principle

A

plasticity in response to one training experience can enhance the acquisition of similar behaviours

22
Q

what is the interference principle

A

plasticity in response to one experience can interfere with the acquisition of other behaviours

23
Q

what are possible post-lesional physiological changes

A

oedema
diaschisis
excitotoxicity
apoptosis

24
Q

what is excitotoxicity

A

cells die releasing neurotransmitters increasing area of issue

25
what is apoptosis
oedema resolves spontaneous recovery occurs larger area affected by stroke loss of ability to communicate as oedema reduces should regain these cells
26
what are the mechanisms for injury induced plasticity
denervation hypersensitivity synaptic hypereffectiveness unmasking silent synapses regenerative synaptogenesis reactive synaptogenesis
27
what is denervation hypersensitivity
where nerves lost connections are easier to generate reaction potential due to reduced polarity
28
what is synaptic hypereffectiveness
at synpase point takes smaller amount of neurotransmitter and fewer connections
29
what is unmasking silent synapses
no longer live connections in these areas but are able to make better use of these
30
what is regenerative synaptogenesis
reestablishing synapse so where one synapse connected try and maximise connections and find pathways to regain function
31
when may motor learning through plasticity have constraints
process of automatisation can be harder with parkinson's disease cognitive impairment may prevent use explicit learning mechanisms cerebellar impairment may prevent use of sensorimotor adaptation