learning and memory Flashcards

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1
Q

define learning.

A

response of the brain to environmental events and involves adaptive changes in synaptic connectivity which will alter behaviour.

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2
Q

describe Hebbs hypothesis for how the brain processes and stores information.

A

‘when an axon of cell A is near enough to excite cell B and repeatedly or persistently takes part in firing it, some growth process or metabolic change takes place in one or both cells such that A’s efficiency, as one of the cells firing B is increased.

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3
Q

wha part of the Brian is associated with memory?

A

hippocampus.

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4
Q

give an example of Hebbs hypothesis.

A

if association between sight of adult A and their smell of perfume is repeatedly made, synapses of A and B onto hippocampul neurone will be strengthened, so that individual inputs are strong to fire the hippocampul neurone, and just the smell of perfume or picture of adult A is sufficient to recall a memory.

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5
Q

define long-term potentiation.

A

mechanism underlying synaptic strengthening.

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6
Q

one high frequency electrical stimulation means what for the LTP?

A

LTP lasts hours

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7
Q

multiple high frequency stimulation means what for the LTP?

A

LTP lasts days/months

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8
Q

state LTP properties.

A

temporal - summation of inputs reaches a stimulus threshold that leads to induction of LTP.
associative - simultaneous stimulation of a strong and weak pathway induces LTP at both pathways (spatial summation)
input specific - LTP at one synapse is not propagated to adjacent synapses.

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9
Q

what is happening at the synapse?

A
  • glutamate release onto inactive cell (RMP)
  • AMPA receptor activated to create EPSP.
  • NMDA receptor blocked by Mg2+ ion.
  • depolarisation for AMPA activation not sufficient to Mg2+.
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10
Q

what happens at the synapse when glutamate is released onto active cell?

A
  • AMPA receptor activated
  • Mg2+ block on NMDA receptor relived
  • Na+ through AMPA and NMDA channels
  • Ca+ through NMDA channel
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11
Q

Ca2+ entry through NMDA receptor leads to…

A
  • activation of calcium calmodulin-dependent protein kinase 11.
    1. phosphorylates existing AMPA receptors increasing their effectiveness
    2. stimulates the insertion of new AMPA receptors into the membrane
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12
Q

Ca2+ entry through NMDA leads to activation of CaMK11, describe this process.

A
  • CaMKII has autocatalytic activity
  • when phosphorylated is constitutively activate (no longer requires Ca2+)
  • maintains phosphorylation, insertion of AMPA receptors, after the depolarising stimulus has receded
  • molecular switch which maintains increased excitability of neurone for minutes to hours.
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13
Q

describe presynaptic events in LTP.

A
  • postsynaptic neurone can feedback to presynaptic neurone by retrograde NT - nitric oxide (NO).
    1. Ca2+ through NMDA channel activates NO synthase
    2. NO diffuses from site of production and activates guanylyl cyclase in pre-synaptic terminal
    3. guanylyl cyclase produces the second messenger cGMP
    4. single transduction cascade leads to increased glutamate release from synaptic bouton.
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14
Q

describe the late phase LTP.

A
  • protein synthesis required for long-lasting LTP
  • protein synthesis inhibitors prevents consolidation of LT memories and LTP.
  • protein synthesis inhibitor injected just post-acquisition inhibit recall
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15
Q

state stages of memory formation.

A
  • acquisition
  • consolidation
  • recall
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16
Q

early phase LTP lasts a minute to an hour, explained by the actions of…

A

Ca2+ through NMDA receptor and subsequent enhancement of AMPA receptor efficiency, pre-syn event etc

17
Q

late phase LTP lasts hours, days or months, requires…

A

new protein synthesis and can involve morphological changes and the establishment of new synapses

18
Q

titanic stimulation leads to…

A

development of new synaptic connections .

19
Q

describe LTD.

A

LTP created in slice preparations by HFS.

LFS causes the opposite (decrease in EPSP amplitude on further stimulation).

20
Q

what happens during LTD.

A
  • NMDA dependent process

- AMPA receptors are dephophorylated and removed from membrane.

21
Q

name parameters to the Morris water maze experiment

A
  • escape latency (training) (time it gets to platform)
  • time in quadant (probe trial) (time it takes swimming)
  • annulus crossings
22
Q

name the findings from Morris’ water maze study.

A

rats with hippocampus lesions are slower at reaching the platform, not improving trial to trial (no memory for previous trial)

23
Q

describe the role of NMDA in LTP and learning.

A
  • NMDA antagonist (APS) no evidence for learning of LTP

- impairment of learning and blockade of LTP by N-metyl-D-asparate receptor antagonist, APS.

24
Q

are studies on animals relevant to humans?

A
  • can’t use humans in brain studies due to ethics, makes it difficult to generalise to humans.
  • use brain surgery patients
25
Q

describe theta rhythms role in learning and memory.

A
  • hippocampul theta activity accompanies behaviours such as head movements and spatially orientated responses in the rat.
  • seems to play a role in synchronising activity in different brain regions.
26
Q

what are waves of neuronal activity (theta rhythms) involved in?

A
  • involved in arousal, alertness, sure during exploration etc.
27
Q

depolarising stimulation coincident with (peak/trough) of waves generates LTP.

A

peak = LTP, trough generates LTD.

28
Q

give evidence that manipulating LTP can increase learning and memory.

A

enhance LTP genetically - increased amounts of type of NMDA receptor (NR28) enhances LTP.
provide enriched environment - enhanced acquisition I Morris’ water maze, potential LTP.

29
Q

how is memory and LTP diminished?

A

age:

  • decreased acquisition in Morris’ water maze
  • decrease LTP
  • decreased expression of NMDA receptors
30
Q

give evidence for reversal of ageing effects by enrichment of a spatial maze task.

A

aged mice in impoverished environment show greater deficits than those in normal or enriched environments.

31
Q

describe associative LTP.

A
  • associative learning/ classical conditioning

- neuronal activity of conditioned fear: LA, CE, CG, LH, PVN

32
Q

describe neuronal mechanisms underlying conditioned fear.

A
  • synaptic connections in amygdala
  • ideal connectivity for LTP to occur
  • strong input from US = depolarisation of post-syn cell
  • weak input from CS = ‘strengthened’ by post-syn depolarisation leading to activation of NMDA receptors, leading to LTP of this synapse.
33
Q

give evidence that optogentics provides proof that LTP underlies fear memories.

A
  • synaptic activation in LA necessary for fear association
  • LTD inactivates and LTP reactivates memory
  • invoking LTP/LTD strengthens/ weakens memory
34
Q

what has been found from the search of cognitive enhancers?

A
  • increasing NMDA function in forebrain leads to improved spatial memory
  • ‘doggre mice’ - NMDA transgenic mouse with activity restricted to forebrain performed better than normal mice in Morris’ study.
35
Q

too much glutamate is…

A

excitotoxic