Learning Theory Application Flashcards

1
Q

What do we try and maximise and minimise in decision making - expand

A
  • maximise gains and minimise losses
  • Decision-making is related to the ability (or inability) to delay gratification and to impulsivity,
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2
Q

Communication between neurons to send message to brain - exlpain

A
  • cell releases a chemincal (neurotransmitter) into the space seperating two cells called SYNAPSE.

-Neurotransmitter corsses synapse and attaches to proteins (receptors) on the receiving brain cell

  • causes changes in the recieving brain cell and message is delivered
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3
Q

GABA (gamma-aminobutyric acid) neurotransmitter

A

Transmit an inhibitory ‘message’ to other
neurons

This type of message would ‘silence’ other neurons

It regulates brain activity to prevent problems in the areas of anxiety, irritability, concentration, sleep, seizures and depression.

Refer slide 8-9 Learning teory application lecture 1

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4
Q

Glutamate neurotransmitter

A
  • Major excitatory neurotransmitter in the central nervous system.

Glutamate plays a major role in shaping learning and memory

Glutamate is essential for normal brain function, and is involved in learning and memory

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5
Q

What is the basal ganglia

A

The basal ganglia are like a ‘gate’ that normally inhibit movements, and allow only some motor commands to be performed

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6
Q

The classical basal ganglia model of action selection model

A
  1. Cortex
    - The cortex sends a motor command.
  2. The basal ganglia
    - (a collection of interconnected nuclei in the midbrain) ‘select’ or ‘inhibit’ the motor plan
  3. Thalamus
    The thalamus is normally constantly inhibited, which will prevent any motor command from being performed. Occasionally, the basal ganglia may disinhibit it and allow a motor command to be performed.
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7
Q

The direct ‘Go’ Path

A
  1. Cortex
  2. Striatum
  3. GPi, SNr (don’t need to remeber the name of these 2)
  4. Thalamus

The basal ganglia releases the thalamus from inhibition, allowing the motor command to be performed.

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8
Q

The indirect ‘no-go’ pathway

A
  1. Cortex
  2. Striatum, GPe, STN
  3. Thalamus - blocked

The basal ganglia further inhibit the thalamus to prevent that action from being performed.

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9
Q

Where does the classical basal ganglia model connect mostly from

A

The striatum

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10
Q

Example of direct pathway: donut

A

Imagine you eat the donuts and it feels satisfying (this is experienced as a reward). Rewards cause bursts in dopamine activity in the basal ganglia and this reinforces the direct pathway connections so it is more likely that this action will be repeated in the future.

  1. Reward
  2. Higher dopamine
  3. Direct pathway connections are strengthened
  4. Action more likely to be repeated in the future
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11
Q

Example of indirect pathway: donute

A

Imagine you eat the donuts and you feel guilt (this is experienced as a punishment). Punishments cause decreases in dopamine activity in the basal ganglia and this reinforces the indirect pathway connections so it is less likely that this action will be repeated in the future.

  1. Punishment
  2. Lower dopamine
  3. Indirect pathway connections are strengthened
  4. Action less likely to be repeated in the future
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12
Q

Dopamine D1 receptors

A
  • only high levels of dopamine activate D1 receptors (they have low affinity to dopamine, i.e., they are not very ‘sensitive’ to it)
  • experiencing rewards results in dopamine bursts
  • dopamine bursts result in D1-mediated long-term potentiation (this is a type of neuroplasticity that strengthens the synapses, or connections, between neurons, so ‘messages’ between them are transmitted more efficiently)
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13
Q

Long-term potentiation from Dopamine D1

A

Repeated synchronous firing increases the strength of the connections between two neurons.
Long-term potentiation is a type of synaptic plasticity that increases the efficacy of neurotransmission.

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14
Q

Dopamine D2 receptors

A
  • only low levels of dopamine activate D2 receptors (they have high affinity for dopamine; high levels of dopamine inhibit them)
  • experiencing punishment results in dopamine ‘dips’
  • dopamine dips result in D2-mediated long-term potentiation
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15
Q

What is gene expression?

A

The DRD1 gene is a gene that contains the recipe for the dopamine D1 receptor.

The DRD2 gene is a gene that contains the recipe for the dopamine D2 receptor.

Not all cells express these genes (meaning not all cells use these recipes to produce these types of receptor).

But some cells do, and they might have a ‘preference’ for expressing one gene or the other, meaning some cells are more likely to express DRD1 whereas others are more likely to express DRD2.

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16
Q

One of the tests that measure Go and No-Go learning

A
  1. Trial: Pick a symbol and then recieve feedback - a correct or incorrect choice
    - learn by trial and error on which symbols to pick and which to avoid
  2. training contingencies (which answers are more ‘correct then others’

3.Test (no feedback given)

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17
Q

Classical basal ganglia model of action selection:

A

The cortex sends motor commands. The basal ganglia select or inhibit these motor plans:
- The direct pathway disinhibits the thalamus, allowing the motor command to be performed.
- The indirect pathway further inhibits the thalamus, preventing the motor command from
being performed.

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18
Q

Learning in the basal ganglia:

A

Actions that are followed by positive feedback or reward:

  • Rewards cause dopamine ‘bursts’ that strengthen the direct pathway via dopamine D1
    receptors.
    So rewarded actions are more likely to be performed in the future.

Actions that are followed by negative feedback or punishment:

  • Punishments cause dopamine ‘dips’ that strengthen the indirect pathway via dopamine D2
    receptors.
    So punished actions are less likely to be performed in the future.
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19
Q

Pharmacological manipulations in healthy individuals:

A

Drugs that increase dopamine release improve learning from positive feedback
(i.e., learning
to adopt an advantageous action, which should rely on the direct pathway)

but disrupt learning
from negative feedback
(i.e., learn to avoid unfavourable actions, which should rely on the indirect pathway).

  • Drugs that decrease dopamine release have the opposite effect: they disrupt learning from
    positive feedback and improve learning from negative feedback.
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20
Q

Genetic individual differences (genotypes):

A
  • Individuals with genotypes associated with increased dopamine neurotransmission via D1
    receptors show better learning from positive feedback (which should rely on the direct pathway).
  • Individuals with genotypes associated with increased dopamine neurotransmission via D2
    receptors show better learning from negative feedback (which should rely on the indirect
    pathway).
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21
Q

Older individuals (dopamine)

A

Because ageing is accompanied by dopamine depletion, decision-making that relies on the direct
the pathway is impaired.

Older individuals have more difficulty learning from positive feedback, but their ability to learn from negative feedback is spared.

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22
Q

Parkinson’s disease:

A

This disease is characterised by dopamine depletion, so non-medicated patients show a pattern
similar to older individuals: difficulty learning from positive feedback, but spared learning from
negative feedback.

Dopamine agonist medication reverses this pattern, improving learning from
positive feedback, but impairing learning from negative feedback. This might explain medication-
induced impulsivity.

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23
Q

Tourette syndrome:

A

This disease is characterised by excess dopamine in the midbrain, so non-medicated patients show good learning from positive feedback, but impaired learning from negative feedback
(which might explain why they are more likely to be impulsive).

Dopamine antagonist medication
reverses this pattern, improving learning from negative feedback, but impairing learning from
positive feedback.

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24
Q

Repetitive behaviours or thoughts as extreme habits are triggered by ______

A

particular stimuli

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25
Q

Habits can have _______ __ ________ components

A

motor and congitive

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26
Q

Within OCD what is another cause of extreme habbits apart from repetitive behaviours

A

Obsessions such as the fear of doing something and the inability to stop having these unpleasant thoughts (ego-dystonic repetitive thoughts)

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27
Q

Which disorders have excesive midbrain dopamine levels

A

Tourette syndrome, autism and OCD

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28
Q

What do amphetamine and cocain do to your dopamine and behaviours

A

Increase dopamine and cause hyperactivity and compulsive and stereotypical behaviours

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29
Q

Imbalance: Direct > Indirect (eg. due to excess dopamine)

A

Fewer of these action plans are inhibited by the indirect pathway so more are performed
(some of which might be completely
irrelevant or useless in the current context).

Performed action plans are also meant to end (be performed once only) and a weaker indirect pathway might not be able to terminate a motor program and stop its
repetition.

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30
Q

What are stereotypical behaviour in animals

A

Excessive grooming:
- Paw licking: Can lead to blisters
- Biting fingers nails

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31
Q

How can we disrupt the indirect pathway in monkeys so they can complete a motor functions they wouldn’t do (Finger Biting)

A

Injecting a GABA antagonist in the GPe

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32
Q

What happens when you inject a monday in the Anterior GPe VS Posterior Gpe

A

Anterior:
- repeatedly performing the same behaviour
(unable to ‘exit a loop’)
- akin to tics, compulsions in humans

Posterior:
- allowing all behaviours to be performed despite their irrelevance + what lookslike disrupted attention
(monkeys made many errors on the food retrieval taskrepeatedly going back to locations where they had
already collected food and were now empty)

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33
Q

how do individuals best learn with OCD and Tourettes

A

Learn less from punishment and more from reward in an unmedicated state.

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