Consolidation and Synaptic Plasticity Flashcards

1
Q

what are the three stages of visual memory?

A

immediate memory, STM, and LTM

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2
Q

how is memory able to become consolidated?

A

if it follows the process of acquisition, STM, LTM

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3
Q

what happens if there is a rapid decay of STM?

A

this can lead to insufficient retrieval and recall

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4
Q

what are the two types of memory systems within the brain?

A

declarative and non-declarative

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5
Q

declarative memory

A

consists of explicit facts and events that we are consciously aware of

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6
Q

non-declarative memory

A

consists of implicit skills and habits, classical conditioning, priming, and non-associative learning

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7
Q

what is one of the main mechanisms of memory consolidation?

A

de novo protein synthesis creates memories

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8
Q

what is the role of RNA?

A

RNA aids in the synthesis of proteins.

when RNA is impaired by toxins introduced into the amygdala, it does not impact STM but impairs LTM

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9
Q

what does antisense technology do?

A

blocks the translation of RNA and the subsequent synthesis of proteins

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10
Q

what are NMDA receptors required for?

A

learning and memory acquisition

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11
Q

what is the connection between NMDA and arc?

A

NMDA receptors lead to the synthesis of the protein arc

in areas of the brain where learning takes place, there is a higher amount of arc protein

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12
Q

evidence of other proteins being important for memory consolidation

A

protein BDNF was expressed differently in epilepsy, which has links to memory deficits

by remediating BDNF expression, memory deficits in epilepsy can be improved

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13
Q

why is it important to only consolidate ‘acquired’ and important memories?

A

because learning and memory are extremely energy intensive

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14
Q

what does the slow integration of memory consolidation into the LTM allow for?

A

more selectivity and categorisation of memories, to make them more easily remembered

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15
Q

what did hebb propose?

A

the idea of synaptic plasticity and ‘neurones that wire together, fire together’

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16
Q

what was historically believed about the function of synapses?

A

to transfer information across neurones

17
Q

what does the dynamic process of synaptic plasticity allow?

A

individuals to change and acquire new functions, particularly in relation to behaviour, learning, and memory

18
Q

what is synaptic plasticity?

A

alteration in the strength of a synapse

19
Q

what is synaptic strength?

A

how likely it is that a postsynaptic neurone will be activated by the same level of presynaptic input

20
Q

how have neurobiological developments found evidence of synaptic plasticity?

A

they can change strength due to different activity between pathways

this is central to understanding learning and memory

21
Q

what is important for processing in the brain?

A

the transfer of information across a network

by linking neurones together in a particular configuration, memories are able to be stored

22
Q

what are the different types of neurones?

A

excitatory or inhbitory

23
Q

excitatory neurones

A

activate the next neurone

24
Q

inhibitory neurones

A

deactivate the next neurone

25
Q

what is long-term potentiation?

A

a long-lasting increase in synaptic strength, e.g., a baby laughing more when being tickled

26
Q

LTP- what happens when pathways are repeatedly stimulated?

A

the EPSP (excitatory postsynaptic potential) is strengthened, which is useful for storing memory

27
Q

what looks similar to the distinction between STM and LTM?

A

early long-term potentiation (E-LTP) AND late long-term potentiation (L-LTP)

28
Q

what are the two types of LTP?

A

non-associative LTP and associative LTP

29
Q

non-associative LTP

A

stimulates neurones, and this intense stimulation strengthens the connection

results in a greater output

30
Q

associative LTP

A

this occurs when there is both high intense and normal stimulation from two inputs

results in strengthening the synapse and input

31
Q

what is the difference between L-LTP and E-LTP?

A

L-LTP requires protein synthesis, whereas E-LTP does not

this shows the importance of protein synthesis in consolidating long-term memories

32
Q

connection between NMDA and LTP

A

NMDA receptors block E-LTP and L-LTP in the same way as STM and LTM

33
Q

where can be LTP be induced?

A

in the amygdala

LTP requires protein synthesis and NMDA receptors

34
Q

evidence of similar mechanisms between LTP and memory consolidation

A

LTP stimulation in the amygdala upregulated the expression of arc in the amygdala

caused higher activity of memory and learning

35
Q

evidence of fear conditoning within mice

A

mice had the brain effect of being presented with a ‘foot shock, resulting in synaptic plasticity and LTP at the synapse

artificially wiring neurones together can construct fake memories

36
Q

what is LTD?

A

a long-lasting decrease in synaptic strength, e.g., baby laughing less after being tickled

37
Q

where is LTD found?

A

most commonly observed in the cerebellum, meaning it may underlie motor learning

38
Q

difference between LTP and LTD

A

high-frequency intense stimulation leads to an increased response to stimulation
vs
low-frequency stimulation leads to a decreased response to test stimulation

39
Q

can LTP and LTD coexist in the same brain areas?

A

yes, and they can lead to increased responding

decreasing inhibition levels will result in higher activity