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PSY2013- Biological Psychology with Research Methods 2 > 4- Declarative Learning > Flashcards

4- Declarative Learning Flashcards

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1
Q

What does declarative learning look at?

A

Cellular and molecular bases of long-term memory

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2
Q

What is the crucial brain structure involved in declarative memory?

A

The hippocampus

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3
Q

What was one of the first brain structures to develop?

A

The hippocampus

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4
Q

What structure do all animals share?

A

The hippocampus

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5
Q

What is the key role of the hippocampus?

A

Forming new memories

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6
Q

What 3 mechanisms are controlled by the hippocampus?

A

Long-term potentiation
Long-term depression
cAMP-response-element-binding regulated protein

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7
Q

Why was HM studied?

A

Couldn’t form any new memories

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8
Q

When does long-term potentiation (LTP) occur?

A

With high frequency stimulation of CA1 neurons via Schaffer collaterals

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9
Q

When are Schaffer collaterals stimulated?

A

When taking in new information

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10
Q

What is the main mechanism used in LTP?

A

Glutamatergic synapses

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11
Q

Which neurotransmitter is used by glutamatergic synapses?

A

Glutamate

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12
Q

What characterises glutamate?

A

As the most common excitatory neurotransmitter in the CNS

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13
Q

What are the 2 types of glutamate postsynaptic receptors?

A

AMPA receptors and NMDA receptors

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14
Q

How is the LTP glutamatergic mechanism started?

A

By frequent presynaptic action potentials

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15
Q

What does the frequent presynaptic action potentials cause in LTP?

A

Strong glutamate release

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16
Q

How is postsynaptic depolarisation (increase in sodium ions) caused in LTP?

A

Glutamate binding to AMPA receptors

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17
Q

How does unblocking occur in LTP?

A

Glutamate binds to NMDA receptors

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18
Q

What is created by a strong Ca2+ influx? (LTP)

A

Protein kinase

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19
Q

What is the fast mechanism involved in protein kinase creation? (LTP)

A

Relocation of new AMPA receptors to postsynaptic

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20
Q

What is the slow mechanism involved in protein kinase creation (LTP)?

A

Activating gene transcription

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21
Q

What 2 processes are triggered when gene transcription is activated? (LTP)

A

Protein synthesis and synapse sprouting

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22
Q

What is the overall response from glutamatergic synapses in long-term potentiation?

A

More efficient connection

23
Q

What is a second mechanism involved in long-term potentiation?

A

Protein synthesis

24
Q

What is the main aspect of the protein synthesis mechanism? (LTP)

A

A strong calcium ion influx creating protein kinase

25
Q

Why is the protein synthesis mechanism slow? (LTP)

A

Gene transcription is activated via phosphorylating transcription factors

26
Q

What experimental evidence demonstrates protein synthesis in long-term potentiation?

A

Inhibiting protein synthesis means more postsynaptic potentials are excited

27
Q

What is the third mechanism of long-term potentiation?

A

cAMP-response-element-binding transcription factor (CREB)

28
Q

What are the 3 processes involved in the CREB mechanism? (LTP)

A
  1. CREB-2 represses transcription
  2. CREB-1 replaces CREB-2
  3. Protein kinase A activates CREB-1 to cause transcription
29
Q

What is the fourth mechanism of long-term potentiation?

A

Transcription

30
Q

What experimental evidence demonstrates transcription in LTP?

A

Knocking out CREB transcription factor

31
Q

What was found by knocking out a CREB transcription factor? (LTP)

A

Long-term but not short-term spatial memory was impaired

32
Q

When does long-term depression (LTD) occur?

A

In low frequency stimulation of CA1 neurons via Schaffer collaterals

33
Q

What cause does long-term depression have?

A

Not be able to effectively learn long-term

34
Q

What is the mechanism of LTD?

A

Glutamatergic synapses

35
Q

How does the glutamatergic mechanism of LTD begin?

A

Rare presynaptic action potentials causing reduced firing

36
Q

What is caused by rare presynaptic action potentials? (LTD)

A

Weak release of glutamate

37
Q

How is postsynaptic depolarisation caused? (LTD)

A

Glu binding to AMPA receptors

38
Q

What does a weak influx of Ca2+ create? (LTD)

A

Protein phosphate

39
Q

What does protein phosphate creation cause? (LTD)

A

Internalisation of AMPA receptors from postsynaptic membrane

40
Q

What is the result of the glutamatergic synapse mechanism of LTD?

A

Less efficient connection

41
Q

What is the cause of more activation and more distribution?

A

We are more likely to link information long-term

42
Q

Why do we remember a stimulus?

A

Neurons encode a stimulus

43
Q

Why do we have a problem recognising competing inputs?

A

None are able to elicit an action potential

44
Q

How do we learn to recognise stimuli?

A

We pay attention to a certain stimulus

45
Q

When is LPD created by competing inputs?

A

One stimulus is recognised on its own

46
Q

When is LTP created by competing inputs?

A

Other two stimuli are cooperative

47
Q

Why can the first stimulus not elicit a response?

A

Due to LDP

48
Q

Why can the other two stimuli alone not elicit a response?

A

Due to LTP

49
Q

What are important mechanisms underlying synaptic plasticity?

A

LTP and LTD

50
Q

How do LTP and LTD underlie synaptic plasticity?

A

Via controlling Ca2+ influx, creating protein kinase/photophatase balance

51
Q

What is there with a high frequency/correlated stimulus, and what does this cause?

A

Unblocked NMDA receptor, causes Ca2+ influx that produces kinase

52
Q

What response is there with a high frequency/correlated stimulus?

A

A more efficient connection

53
Q

What is there with a low frequency/uncorrelated stimulus and what does this cause?

A

Blocked NMDA receptor, causes decreased Ca2+ influx that produces phosphataese

54
Q

What response is there with a low frequency/uncorrelated stimulus?

A

A less efficient connection

PSY2013- Biological Psychology with Research Methods 2 (22 decks)

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