memory, LTP and LDP mechanisms Flashcards

1
Q

Learning

A

acquisition of information

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2
Q

Memory

A

storage of learned information

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3
Q

Recall

A

reacquisition of stored information

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4
Q

The engram

A

physical embodiment of a memory

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5
Q

Procedural memory

A

Skills and associations largely unavailable to conscious mind
e.g riding bike

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6
Q

Declarative memory

A

Available to conscious mind. Can be encoded in symbols and language

e.g capital of france

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7
Q

Explicit memory

A

memory that can be consciously recalled (e.g. recalling riding a shiny new bike on the Christmas day when you were 5)

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8
Q

Implicit memory

A

memory that cannot consciously recalled (e.g. learning to ride a bike). Can be different types:
- Procedural memory
- Classical conditioning
- Priming (when one stimulus influences the response to subsequent stimuli)

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9
Q

Priming

A

when one stimulus influences the response to subsequent stimuli

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10
Q

advantages of using lower vertebrates as models for simple systems

A
  • neuronal size
  • circuit complexity
  • temperature dependence
    • switches neurones on/off
  • mapping tools
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11
Q

simple forms of memory

A

habituation = desensitisation
sensitisation

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12
Q

what is habituation

A

desensitisation of response to stimuli
- amplitude of response reduces if stimulus is repeated
- of eye blink reflex
- of repetitive non-harmful stimulus presentation
- of visual attention
- of emotional response

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13
Q

what is sensitisation

A

increases amplitude of response over time

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14
Q

what do studies of aplysia gill withdrawal reflex show?

A
  • Touch or water jet causes gill withdrawal
    • contains sensory neurones
  • Habituation to repeated stimuli
  • 10-15 touches at 10-20 sec interval reduces the reflex
  • sensory neurone (siphon skin) → motor neurone (gill muscle)
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15
Q

origins of habituation

A
  • pre-s neurone = regular amplitude of neurone firing
  • post-s neurone = declining amplitude of neurone firing

⇒ origin is somewhere between pre and post synaptic neurone

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16
Q

what is the mechanism of habituation (desensitisation)

A
  • caused by reduced transmitter release / depletion of readily releasable pool
  • less vesicles available in active zone to be released = less aplitude
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17
Q

what is the readily releasable pool

A

what is released immediately when post-s depolarises (active zone)

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18
Q

what is the reserve pool

A

spare vesicles and NTs that require high depolarisation to be released

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19
Q

explain how desensitisation (habituation occurs)

A

when you stimulate specific neurones repeatedly, the amount of vesicles available to transmit neurotransmitters is depleted requiring higher stimulus to use reserves -> meaning there are weaker signals sent as a result

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20
Q

how does sensitisation occur

A

L29 sensitising neurone releases serotonin → activates adenylyl cyclase → cAMP → PKA → phosphorylation of ion channels including K channels -> longer depolarisation period = sensitised

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21
Q

habituation and sensitisaiton summed up in a sentence

A

Habituation: depletion of the synaptic vesicle pool
Sensitisation: serotoninergic feedback from other sensory neuron

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22
Q

how does associative learning occur in a simple model

A

when L29 has an EPSP -> other sensory neurones around can be depolarised causing increased depolarisation of nearby neurones

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23
Q

what do the mechanisms of sensitisation and conditioning typically involve

A
  • Multiple intracellular signalling pathways
  • Pre and post-synaptic
  • Long term involves the nucleus
    • requires changes to gene expression
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24
Q

what enzymes are involved in early stages of associative learning

A
  • PK2
    • activated by Ca
  • PKa
    • activated by cAMP?
  • PKC
    • activated by diceglycerol
  • produced by G proteins/channels
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25
Q

what molecule activates PK2

A

Ca

26
Q

what molecule activates PKA

A

cAMP

27
Q

what molecule activates PKC

A

diglycerol

28
Q

what enzymes are involved in late stages of associative learning

A
  • MAP kinase
    • travels from cytoplasm → nucleus and phosphorylates TF → gene expression
    • proteins are transported to synapse
    • establishes longer response
29
Q

what is the concept of hebbian synapse

A

Coordinated activity of a presynaptic terminal and a postsynaptic neuron strengthen the synaptic connections between them
ie neurones that fire together wire together

30
Q

major role of hippocampus

A

→ spatial memory formation

31
Q

structure of hippocampus

A
  • many layers
  • input from entorhinal cortex
  • dentate gyrus -> CA3 contains mossy fibres
  • CA3 -> CA1 contains schaffer colaterals
  • neuronal output via fornix and subiculum
32
Q

what is cooperativity

A

Cooperativity refers to the need to stimulate multiple afferent fibers to induce LTP

33
Q

what have experiments shown about LTP

A
  • ca3-ca1 synapses are glutaminergic
  • high freq stim (1000Hz) produces long lasting potentiation → increased firing rate
34
Q

types of glutamate receptors

A

AMPAR
- opens = depolarises cell
- Na+

mGluR
- metabotropic

NMDA
- Ca2+
- v-dependent Mg2+ block
- phosphorylation

35
Q

how do NMDA glutamate channels work

A
  • Ca2+ channel
  • activates kinases
  • phosphorylates proteins to increase EPSP
  • requires depolarisation to remove v-dependent magnesium block
36
Q

how does early phase LTP work

A
  • NMDAR mediated Ca activates calmodulin kinase II
  • autophosphorylation and activation triggered by Ca
  • phosphorylation enhances AMPA currents
  • increased potentiaion = increased currents
37
Q

what is AMPAfication

A
  • pre-s excitatory signals causes delivery of ready-prepared AMPA receptors to the synapse, increasing EPSP
38
Q

how does late stage LTP work

A
  • long term storage requires protein synthesis
  • cAMP → PKA → activates proteins and phos proteins in nucleus
  • CREB binds to CRE to stimulate phosphorylation of CREB transcription
39
Q

impact of LTP on memory formation

A

inhibiting LTP inhibits some memory formation

40
Q

which mutations/drugs can affect learning

A

Mutations of CaMKII, NMDARs, cAMP pathway all affect aspects of learning

41
Q

inputs and outputs of cerebellum

A

+ve inputs = mossy and climbing fibres (efferent)
-ve outputs = purkinje cells

42
Q

synapses of climbing fibre

A

climbing fibre has multiple synapses on 1-10 purkinje cells1 climbing:1-10 purkinjes

43
Q

synapses of mossy fibre

A

mossy fibres synapse onto 1 granule cell and contact 1000 purkinje neurones
1 mossy:1 granule(parallel):splits to contact 1000s purkinjes

44
Q

do mossy or climbing fibres form stronger synapses?

A

climbing fibres, becuase its 1:1, not 1:1:1

45
Q

what does activation of a climbing fibre do

A

depolarisation of purkinje cell

46
Q

how to measure purkinje synapses

A
  • recording purkinje cell response to parallel fibre = measure EPSP amplitude
  • stimulate parallel fibre simultaneously = changes in synapse and decrease in amplitude of EPSP
47
Q

which glut channels are involved in cerebellar LTD

A
  • metabotropic Glutamate receptors, AMPA-R and V-gated Ca2+ channels - not NMDA
48
Q

types of synapses in cerebellar long term depression

A

climbing:purkinje = AMPA receptors

granule/parallel:purkinje = metabotropic glutamate receptors

  • stimulate only parallel fibre = not much PKC activated
  • stimulate climbing + parallel = lots of AMPA activation → strong depolarisation of purkinje cell → V gated Ca2+ increased ic[Ca2+] → Ca2+ increases activity of PKC
49
Q

difference between climbing and parallel fibres

A

Climbing fiber synapses contact spines on the primary Purkinje cell dendrite, whereas parallel fiber synapses contact spines on secondary and tertiary dendritic branches

50
Q

how does long term depression occur in cerebellum?

A
  1. climbing + parallel increases PKC activity due to Ca2+
  2. PKC phosphorylates AMPA GluR2 subunit
  3. causes AMPA receptors to be endocytosed
  4. reduced EPSP
51
Q

how does long term depression occur in cerebellum?

A
  1. climbing + parallel increases PKC activity due to Ca2+
  2. PKC phosphorylates AMPA GluR2 subunit
  3. causes AMPA receptors to be endocytosed
  4. reduced EPSP
52
Q

can LTD can reverse an LTP?

A

yes via depotentiation

53
Q

how does hippocampal long term depression occur

A
  • synapses become weakened when they are active but the rest of the cell isn’t
  • LTD and LTP are Ca2+ dependent
  • degree of NMDS receptor activation determines probability of inducing LTP or LTD
54
Q

where does hippocampal LTD occur

A
  • occurs at CA3-CA1 neurones synapse
55
Q

what enzymes are activated via LTP

A

kinases

56
Q

what enzymes are activated via LTD

A

phosphatases

57
Q

role of calcium in hippocampal LTD/LTP

A
  • small increases in Ca from NMDA trigger more phosphatase action → reduces AMPAR efficacy
  • large increases in Ca from NMDA activate more protein kinases → increase AMPAR efficacy
58
Q

what is adaptation

A

form of plasticity
change of response to same stimulus

59
Q

what fluorescent proteins show proton release following NT release

A
  • sypHy
    • reporter of neural activity
    • fluorescent when H+ has been exocytosed
60
Q

role of - iGluSnfr protein

A
  • fluorescent reporter of glutamate
    • glutamate changes conformation of protein → bright