consolation and synaptic plasticity - week 2 Flashcards

1
Q

timescales of memory

A

memories can persist for different lengths of time depending on underlying mechanism

memories can be localised to specific areas of the brain, take time to stabalise and are likely to be supported by synaptic plasticity
- pavlovian fear memories in the amygdala

memories can be supported by decreases in synaptic strength
- motor memories in the cerebellum

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2
Q

visual memory

A

can be separated into 3 stages

iconic

short term memory

long term memory

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3
Q

iconic memory

A

less than 1 second

likely to result from brief after images in the sensory neurons of the retinal surface in the eye

demonstrated with the sperling array

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4
Q

short term memory

A

retention of information over a period minutes to hours

poorly defined concept

generally thought that the biological mechanisms of s-t memory commonly include sustained neural activity
- persistent neural activity can sustain STM

in monkeys
- electrophysical recordings showed that the activity of neurons in the visual association inferior temporal cortex which were sensitive to a particular complex visual stimulus actually outlasted the presentation of the stimulus

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5
Q

long term memory

A

can last up to a lifetime (24 hrs)

depends on specific areas within the temporal lobe

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6
Q

fear conditioning

A

type of pavlovian conditioning

includes the formation of an association between a previously meaning stimulus and an aversive outcome

subsequent exposure to the now fear-conditioned stimulus results in fearful behaviour

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7
Q

fear conditioning - what is the main brain area implicated

A

amygdala

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8
Q

encoding long lasting memories

A

persistant neural activity sustains STM eventually this dissipates yet the memory remains intact for much longer

notion that STM is stabilised into a LTM may be inaccurate
- certain studies show that is STM is impaired LTM still forms
- so perhaps the mechanisms of LTM are triggered directly by the learning event in parallel with sustained neural activity

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9
Q

what distinguishes LTM and STM

A

differing dependence upon the synthesis of new proteins

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10
Q

mechanism for memory consolidation

what shows synthesis of protiens is needed for memory consolidation

A

anisomycin - prevents protein synthesis

can be infused directly into brain of rats at levels that almost completely prevent the synthesis of any new protiens for several hours

intra-amygdala infusion of anisomycin before or soon after pavlovian conditioning selectively disrupts LTM while leaving STM intact as shown in fear conditioning

also increased gene expression triggered by learning
- reasonable to suggest that specific protiens encoded by their up regulated genes might be required for consolidation

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11
Q

mechanism for memory consolidation

what protein

A

the activity - related cytoskeletal - associated protein (Arc) is simply up regulated in the amygdala following pavlovian fear conditioning

when synthesis of arc is selectively inhibited in the amygdala, the consolidation of the fear memory impaired

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12
Q

mechanism for memory consolidation

mechanism that translates behaviourally induced electrical signals in brain into gene expression

A

one of the direct regulators of arc expression is the ERK/MAPK signalling pathway

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13
Q

mechanism for memory consolidation

ERK/MAPK signalling pathway

A

this pathway consists of a series of kinases

these are protein enzymes that function to phosphorylate other protiens

this causes their enzymatic function to be activated

leading to the activation of further downstream mechanisms in the pathway

the same study that the upregulation of arc following fear conditioning also showed that this upregulation was dependent upon ERK/MAPK signalling
- as expected the inhibition of ERK/MAPK signalling also impairs the consolidation of fear memories in the amygdala

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14
Q

mechanism for memory consolidation

NMDA receptor

A

glutamatergic receptor

upstream of ERK/MAPK pathway the primary cell surface receptor involved in learning in the NMDA receptor

heavily implicated in learning with links to ERK/MAPK pathway

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15
Q

mechanism for memory consolidation

NMDA receptor - evidence

A

direct infusion of NMDA receptor antagonism AP-5 into the amygdala blocks the acquisition of fear conditioning

blocks LTM
also impairs STM
- suggest NMDA receptor is critically involved in memory acquisition
- divergences downstream mediating STM and LTM

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16
Q

synaptic plasticity

A

alteration in the strength of a synapse

17
Q

long term potentiation

A

persistent enhancement of postsynaptic response

18
Q

long term potentiation

demonstation

A

by lomo in hippocampus of anaesthetised rabbits

19
Q

long term potentiation

basis observation by lomo

A

if one of the pathways into the hippocampus (the perforant pathway terminating in the dentate gyrus) was stimulated at a high frequency
the subsequent response to a test stimulation was increased

importantly this potentiation lasted up to 10 hours after stimulation
- much longer than any sustained activity in studies of visual STM

20
Q

synaptic understanding of pavlovian conditioning in the amygdala to lomo

3 main differences: species

A

behavioural on rabbit

most pavlovian conditioning on rodents

21
Q

synaptic understanding of pavlovian conditioning in the amygdala to lomo

3 main differences: area

A

those on rodents have concentrated on hippocampal LTP

not easy to explain how synaptic potentiation between 2 hippocampal neurons gives rise to the complex spatial and concious memories that are thought to depend on hippocampal processing

22
Q

synaptic understanding of pavlovian conditioning in the amygdala to lomo

3 main differences: associative nature

A

the original LTP observed was non-associative (induced by activity in a single input pathway)

contrats associative LTP (depends on co-activated of two inputs) that is thought to underpin associative learning

associative LTP may be able to explain pavlovian conditioning because it involves 2 neural pathways

23
Q

LTP and memory?

A

similarites between LTP and memory consolidation

stong evidence that LTP is a mechanism of memory

(distinction similar to LTM and STM)

24
Q

LTP and memory

demonstration

A

know that there is synaptic plasticity in the amygdala of rats and mice
- conditioned rats to associate a tone with an adversive footshock then measured both behavioural fear and electrical activity in the amygdala elicited by the tone

the electrophysical response in the lateral amygdala was substantially potentiated after conditioning, and if the conditioning parameters induced a behavioural memory
- unpairing tone and footshock = no synaptic plasticity

25
Q

LTP and memory

underlying mechanism?

A

while the demonstration of behaviourally induced synaptic potentiation strongly suggests plasticity mediates longer term memory

doesnt necessarily follow the associative LTP in the amygdala is the underlying mechanism

26
Q

LTP and memory

technological advances

A

enabled us to demonstrate directly the associative nature of amygdala LTP

can now experimentally activate specific neurons in the amygdala and if this is done at the same time as the presentation of the tone it is possible to artifically induce conditioned fear in a rat that has never been exposed to footshock

therefore consolidation is linked to synpatic plasticity

27
Q

does LTP require protein synthesis

A

yes

stimulation in amygdala upregulated the expression of arc

28
Q

does LTP require NMDA receptors

A

yes

29
Q

long term depression

A

persistant reduction of postsynaptic response

30
Q

long term depression
- why does it happen

A

due to low frequency stimulation

31
Q

can LTP and LTD co exist

A

yes

both can lead to increased responses

depends on where in the circuit

32
Q

where is LTD most commonly associated with ?

A

cerebellum

linked with motor form of learning —> DEBATED

33
Q

LTD at excitatory

A

decrease

34
Q

LTD at inhibitory

A

increase

35
Q

LTP at excitatory

A

increase

36
Q

LTP at inhibitory

A

decrease