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Biological Psychology 2 > Molecular & Cellular Bases > Flashcards

Molecular & Cellular Bases Flashcards

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1
Q

What are the two main forms of learning that can be investigated?

A

Procedural - behaviour change/acquisition. Simple pathways that link sensations to movements. Easy to study.
Declarative - knowledge acquisition (mediated by the hippo). Difficult to study.

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2
Q

What are the two parts of procedural learning?

A

Non-associative learning - habituation, sensitisation.

Associative learning - classical conditioning, operant conditioning.

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3
Q

What is a habituation?

A

Decrease in the strength or occurrence of a behaviour due to the repeated exposure to the stimulus that produces that behaviour.

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4
Q

What is a sensitisation?

A

Increase in the strength or occurrence of a behaviour due to exposure to an arousing/noxious stimulus.

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5
Q

What are the main levels of analysis?

A

Molecular & cellular - behavioural & cognitive neuroscience.
With increased knowledge = increased ethical dilemma.

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6
Q

How did aplysia contribute to non-associative learning (invertebrate models of learning)?

A

Aplysia = snails.
Kandel intensively studied them.
Giant neurons that could be easily isolated to form mini brains.
Gil withdrawal - reflex in aplysia. Stimulation of the siphon leads to a protective/defence reflex to withdraw the gil. Only 2 neurons involved.
Snail learns and new synaptic connections are formed - LTM.

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7
Q

Where does habituation take place?

A

At synapse between sensory and motor neuron.
Neurotransmitter release at pre-synapse gets attenuated. Occurs at post-synapse - post-synapse neuron response gets weaker.

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8
Q

How do chemical synapses work?

A
  1. Vesicle docked at active zone.
  2. AP arrives, voltage gated Ca+ channels open.
  3. Exocytosis occurs - neurotransmitters released into cleft.
  4. Neurotransmitter caused transmitter-gated ion channels to open. Na+ rushes into cell - depolarisation.
  5. Used vesicles are recycled (endocytosis).
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9
Q

Where does sensitisation occur?

A

Sensory neuron and motor neuron synapse.

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10
Q

How does sensitisation occur?

A
  1. AP at terminal button of neutron L29 - release of serotonin.
  2. Serotonin receptors at terminal button of sensory neutron activated - cascade of molecular dynamics - activation of protein kinase A in sensory neuron.
  3. Protein kinase A blocks part of the K+ (potassium) channels in sensory neutron.
  4. Blocking of K+ channels. Prolonged action potentials at terminal button of sensory neuron.
  5. Longer APs - stronger influx of calcium into sensory neuron’s terminal button.
  6. More calcium influx = more vesicles will release NT into synaptic cleft between sensory + motor neurone.
  7. More NTs - stronger response at motor neuron.
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11
Q

Sensitisation shares the same neural mechanism with which process?

A

Classical conditioning.

Quantitative difference - classical > sensitisation.
More amplified neural response.

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12
Q

Who discovered classical conditioning?

A

Pavlov.

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13
Q

Who discovered operant conditioning?

A

Thorndike, Skinner.

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14
Q

How does classical conditioning in the aplysia work?

A

When CS and UCS are paired - Ca(2+) streams into terminal button of sensory neutron when cAMP is synthesised. Much more active protein kinase A than during sensitisation - more K+ channels blocked, longer AP, stronger response at motor neuron.

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15
Q

When does LTP occur in the hippocampus (vertebrate models of learning + memory).

A

LTP occurs with high frequency stimulation of Schaffer collaterals.

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16
Q

What are the 2 types of glutamate-gated ion channels on the post-synaptic membrane?

A

AMPA receptors (sodium channel) and NMDA receptors (sodium + calcium channel).
AP arrives at a Schaffer collateral - glutamate is released.
NMDA receptors - blocked by magnesium ion unless glutamate binds to receptors and post-synaptic is depolarised.
Glutamatergic synapses - using NT glutamate. Excitatory. Most common type in CNS.

17
Q

What does an influx of Ca(2+) trigger?

A

An action potential.

18
Q

Explain how LTPs occur.

A
  1. Simultaneous AP at presynaptic axon terminal buttons - depolarisation of postsynaptic membrane.
  2. Glutamate + depolarisation of dendrite. Magnesium blocks NMDA receptors released - influx of calcium. Calcium = relocation of new AMPA receptors to post-synaptic membrane = increased likelihood that AP will be generated.
  3. More sodium channels at post-synaptic membrane (AMPA) + more vesicles filled with glutamate at terminal button - synapse much more efficient.
19
Q

How does long-term depression occur (vertebrate models of learning + memory)?

A

Low frequency stimulation of Schaffer collaterals = long-term reduction of EPSP in CA1.
Without strong NMDA receptor activity - weak influx of calcium - AMPA receptors are lost (because not being used). Synapse becomes less effective.

20
Q

How does LTP lead to long-term memory?

A

Input has different sensory qualities. Overtime the pairing of these cause an increase response of neutron - LTP.
Frequent pairing - increase in AMPA receptors at postsynaptic membrane.

21
Q

How does LTD relate to long-term memory?

A

Forgetting the memory, undoing the association.

22
Q

What is Hebbian modification?

A

Neurons which fire together, wire together. Neurons which fire out of synch, lose their link.

23
Q

How does Hebbian modification relate to LTPs?

A

Strengthening of cell assemblies through LTP. One part activated = whole assembly activated.

24
Q

What immediate effects does LTP lead to?

A

New AMPA receptors.

25
Q

What delayed effects does LTP lead to?

A

Protein synthesis and regulation of gene transcription.

Both trigger synaptic growth.

26
Q

What do protein synthesis inhibitors do to LTPs?

A

Reduce LTPs.
Protein synthesis = prolongs effect of LTP - TM.
Protein synthesis inhibitors lead to deficits in LTM. Evidence seen in mice (Fioriti).

27
Q

When does protein synthesis occur?

A

During formation of LTM.

28
Q

What is protein synthesis regulated by?

A

CREB (c-AMP response element binding) protein.

29
Q

What does CREB-2 do?

A

Inhibits gene expression.

30
Q

What does CREB-1 do?

A

Displace CREB-2.
Phosphorylated CREB-1 initiates transcription.
Both of these are induced by LTP (long-lasting).

Biological Psychology 2 (11 decks)

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