4- Declarative Learning Flashcards

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
Why is the protein synthesis mechanism slow? (LTP)
Gene transcription is activated via phosphorylating transcription factors
26
What experimental evidence demonstrates protein synthesis in long-term potentiation?
Inhibiting protein synthesis means more postsynaptic potentials are excited
27
What is the third mechanism of long-term potentiation?
cAMP-response-element-binding transcription factor (CREB)
28
What are the 3 processes involved in the CREB mechanism? (LTP)
1. CREB-2 represses transcription 2. CREB-1 replaces CREB-2 3. Protein kinase A activates CREB-1 to cause transcription
29
What is the fourth mechanism of long-term potentiation?
Transcription
30
What experimental evidence demonstrates transcription in LTP?
Knocking out CREB transcription factor
31
What was found by knocking out a CREB transcription factor? (LTP)
Long-term but not short-term spatial memory was impaired
32
When does long-term depression (LTD) occur?
In low frequency stimulation of CA1 neurons via Schaffer collaterals
33
What cause does long-term depression have?
Not be able to effectively learn long-term
34
What is the mechanism of LTD?
Glutamatergic synapses
35
How does the glutamatergic mechanism of LTD begin?
Rare presynaptic action potentials causing reduced firing
36
What is caused by rare presynaptic action potentials? (LTD)
Weak release of glutamate
37
How is postsynaptic depolarisation caused? (LTD)
Glu binding to AMPA receptors
38
What does a weak influx of Ca2+ create? (LTD)
Protein phosphate
39
What does protein phosphate creation cause? (LTD)
Internalisation of AMPA receptors from postsynaptic membrane
40
What is the result of the glutamatergic synapse mechanism of LTD?
Less efficient connection
41
What is the cause of more activation and more distribution?
We are more likely to link information long-term
42
Why do we remember a stimulus?
Neurons encode a stimulus
43
Why do we have a problem recognising competing inputs?
None are able to elicit an action potential
44
How do we learn to recognise stimuli?
We pay attention to a certain stimulus
45
When is LPD created by competing inputs?
One stimulus is recognised on its own
46
When is LTP created by competing inputs?
Other two stimuli are cooperative
47
Why can the first stimulus not elicit a response?
Due to LDP
48
Why can the other two stimuli alone not elicit a response?
Due to LTP
49
What are important mechanisms underlying synaptic plasticity?
LTP and LTD
50
How do LTP and LTD underlie synaptic plasticity?
Via controlling Ca2+ influx, creating protein kinase/photophatase balance
51
What is there with a high frequency/correlated stimulus, and what does this cause?
Unblocked NMDA receptor, causes Ca2+ influx that produces kinase
52
What response is there with a high frequency/correlated stimulus?
A more efficient connection
53
What is there with a low frequency/uncorrelated stimulus and what does this cause?
Blocked NMDA receptor, causes decreased Ca2+ influx that produces phosphataese
54
What response is there with a low frequency/uncorrelated stimulus?
A less efficient connection