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PSC3008 > lecture 21 and 22 - anya hurlbert > Flashcards

lecture 21 and 22 - anya hurlbert Flashcards

1
Q

learning is…

A

the acquisition of new knowledge

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2
Q

memory is…

A

the retention of learned knowledge

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3
Q

memory is stored as a…

A

neural trace (memory must involve changes in connections between neurones)

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4
Q

recall is…

A

reactivation of the trace

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5
Q

forms of memory

A

declarative and procedural

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6
Q

declarative

A
  • records of facts and events
  • accessible to consciousness, easy to forget
  • describe what we know and what we remember about things that have happened to us
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7
Q

procedural

A
  • learned skills and behaviours
  • involved learning a motor response in association with a sensory input
  • inaccessible to consciousness, but never forget
  • cant verbalise is e.g riding a bike
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8
Q

time scale of memory can be

A

short term (STM) - verbal or visuospatial
ling term (LTM)

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9
Q

example of verbal and visuospatial STM

A

verbal - memory of someones phone number
visuospatial - jigsaw puzzle (remembering what piece you need and where it is)

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10
Q

example of LTM

A

visual - people faces
auditory - music

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11
Q

non associative learning in procedural memory:
habituation=

A

learn to ignore
e.g people hear planes going over head who live near to airport and they learn to ignore the sound

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12
Q

sensitisation=

A

learn to intensify
stimuli that normally wouldnt evoke a response suddenly becomes more powerful and causes you to react e.g home alone and you hear a noise

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13
Q

associative learning in procedural memory:
classical conditioning=

A

process by which a neural stimulus becomes associated with a meaningful stimulus
e.g. bell –> food –> salivation
bell –> salivation

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14
Q

instrumental conditioning=

A

process by which a response is gradually learned via reinforcement or punishment
e.g we learn that a behavior produces a particular consequence
if positive –> repeat behavior
if negative –> do no repeat behavior

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15
Q

why are invertebrates used in procedural learning experiments

A
  • simple learning circuits
  • big cells - easy to identify + isolate
  • small systems
  • simple genetics
  • easy to keep alive
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16
Q

which marine invertebrate is mainly used in procedural memory experiments

A

sea slug aplysia californica

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17
Q

why are aplysia used

A
  • simple nervous system
  • gill withdrawal reflex
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18
Q

habituation in aplysia

A

decrease over time in response to repeated stimulus that lacks meaning

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19
Q

sensitisation in aplysia

A

exaggeration in response to normal stimuli after strong stimulus

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20
Q

the gill withdrawal reflex

A

when the water is squirted onto the siphon and detects touch the siphon and gill contract

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21
Q

neuronal circuitry of the gill withdrawal reflex

A

siphon skin –> sensory neurone (24) –> synapse –> motor neurone (6) –> gill muscle

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22
Q

how does the gill withdrawal reflex show habituation

A

repeated stimulation of the siphon skin leads to progressively less contraction of the gill

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23
Q

where is the locus if the habituation

A

the SN - MN synapse.
EPSPs decline as the SN is repeatedly stimulated

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24
Q

this is a form of…

A

homosynaptic depression

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25
Q

is it a pre or post synaptic effect

A

pre as there is fewer quanta (of glutamate) release per AP because there is less calcium entry per AP

26
Q

how does the gill withdrawal reflex show sensitisation

A

an electrical shock to the head or tail sensitises the aplysia and causes a squirt of water to cause a much bigger response (withdrawal of the gill)

27
Q

how does the sensitisation occur

A

when the shock arrives at the head it activates the L29 interneuron that synapses on to the sensory neuron

28
Q

what is released from L29

A

serotonin which causes more calcium to enter per AP and thus more quanta of glutamate per AP
this causes an increases response

29
Q

what is this called

A

heterosynaptic facilitation (as there is an extra synapse)

30
Q

presynaptic mechanisms involved in sensitisation:
5-HT receptor -

A

is G protein coupled and metabotropic which activates cAMP as second messenger

31
Q

cAMP activates two kinases…

A

PKA and PKC which act to enhance release of transmitter

32
Q

how does PKA work

A

phosphorylates and closes K+ channel
this stops potassium leaving the cell whih will keep positive charges in the cell and keep is depolarised for longer broadening the AP, this causes more calcium to enter and more quanta of glutamate per AP

33
Q

how to PKC work

A

acts directly on vesicle release mechanism and causes enhances transmitter release

34
Q

metabotropic receptor (G protein coupled) examples

A

ACh muscarinic
glutamate metabotropic
GABAb
5HT
DA
NE

35
Q

structure of metabotropic receptors

A

7 membrane spanning alpha helices

36
Q

Gs and Gi do what

A

Gs - stimulates effector protein
Gi - inhibits effector protein

37
Q

two effector systems of metabotropic receptors

A

G protein gates ion channels (e.g GABAb couples to K+ channels)
G protein activates enzymes (2nd messenger cascade) (e.g NEbeta receptor activates Gs which increases cAMP, activating PKA)

38
Q

alzheimers - loss and damage to synapses

A

amyloid beta reduces number and plasticity of synapses
modifies tau proteins impair synaptic vesicle release and postsynaptic receptor insertion

39
Q

associative learning =

A

the forming of associations between two events

40
Q

classical conditioning =

A

learning of association between unconditional stimulus (US) (which evokes a response without training) which is predicted by a conditional stimulus (CS) (which does not normally evoke a response)

41
Q

before conditioning:
CS (bell) —-> no response (no salivation)
US (meat) —-> response (salivation)
conditioning:
CS + US (bell, then meat) —-> response (dribble)
after conditioning?

A

CS (bell) —-> response (drool)

42
Q

associative learning in aplysia (conditioning)

A

before:
- CS (siphon stim) - no response
- US (shock to tail) - response
during:
- CS + US -> response
after:
- CS -> response

43
Q

presynaptic facilitation after classical conditioning

A

the US (tail shock) activates interneurons (e.g L29) which release 5-HT onto the SN

44
Q

activity dependent facilitation

A

if the CS (siphon touch) precedes the US, the 5-HT release elicits even stronger presynaptic facilitation

45
Q

coincidence detection in presynaptic mechanisms (classical conditioning)

A

1) weak CS does not initiate response from MN on its own, but it does elicit APs which cause calcium to enter presynaptic terminal of SN
2) calcium activates adenylyl cyclase which acts as a coincidence detector which detects the coincidence of the weak activation of the presynaptic terminal and then the strong activation from the US.
3) strong US causes L29 to release 5-HT onto presynaptic terminal of SN, activation the G protein associated with the 5-HT receptor
4) the G protein further activates the primed adenylyl cyclase
5) the super activated adenylyl cyclase activates cAMP more strongly which activates PKA and PKC
6) kinases have the same effects as in the sensitisation mechanism

46
Q

post synaptic mechanisms in classical conditioning:
1) pairing of the CS and the US leads to strong depolarisation of the…

A

motor neuron

47
Q

the SN releases ________ into the MN

A

glutamate

48
Q

the postsynaptic NMDA receptor in the presence of strong depolarisation is…

A

unblocked (Mg ion is removed) and calcium enters the postsynaptic MN

49
Q

calcium activates a retrograde messenger system that signals the pre synaptic cell to release more transmitter
calcium also activates CAMK II that enhances non-NMDA receptor

A
50
Q

how can classical conditioning phenomenon be mimicked

A

by applying 5-HT to SN (representing the strong US) just after the SN fires APs (representing the weak activity of the CS)

51
Q

after training the weak CS will now elicit a response greater and longer term than from

A

sensitisation

52
Q

this is due to

A

modification of pre synaptic proteins and increased protein synthesis and modification of post synaptic proteins

53
Q

differences between sensitisation and conditioning

A
  • conditioning causes longer lasting and stronger
    enhancement of withdrawal reflex (via the SN-MN) than short term sensitisation does.
  • conditioning requires sequential activation of the SN by the CS and then the US
  • conditioning requires activity of both the SN and the MN
  • both conditioning and sensitisation utilise the same route to increase transmitter release (cAMP activated phosphorylation)
54
Q

unpaired stimuli

A
  • siphon touch and tail shock may be close in time but the former does not reliably predict the other
  • not only is there no sensitisation but depression may occur (EPSP declines over time)
55
Q

paired stimuli

A
  • siphon touch and tail shock are close in time, and the former reliably predicts the latter
  • EPSP response is enhanced
56
Q

time scale of habituation (short term)

A

decrease in response following ~10 stimuli delivered every minute
response recovers after a rest period of several minutes to 1 hour

57
Q

time scale of habituation (long term)

A

four sessions of stimulation, at intervals of several hours to 1 day, leads to habituation response lasting up to 3 weeks
can lead to a decrease in number of synaptic contacts between SN and MN (from 90% of SNs with detectable connections to 30%)

58
Q

mechanisms of short term sensitisation

A

occurs after a single brief training session
- activity dependent presynaptic facilitation which is mediated by the action of PKA
- serotonin binding to its receptor activates G protein which activates cAMP which causes activation of PKA which phosphorylates the potassium channel and theres an increase in depolarization of the membrane which causes an increase in calcium into the cell and an activation of PKC which causes enhanced neurotransmission

59
Q

intermediate term sensitisation

A

same set of mechanisms that happen in classical conditioning
longer application of 5-HT or paired stimulation as in conditioning you can have effects that last for hours
requires both presynaptic and postsynaptic protein modifications
PKA acts on increasing calcium which activates CAMK and PKC
those activations then cause an increase depolarisation on the post synaptic side which causes unblocking of the NMDA receptor and an increase of calcium into the postsynaptic cell which activates the non-NMDA receptor and strengthens the effectiveness of these receptors
also leads to insertion of new postsynaptic receptors

60
Q

long term sensitisation

A

multiple training sessions spaces over several days
PKA migrates to the nucleus and activates a cAMP response element binding protein
this activates a gene transcription pathway leading growth of the synapse
starts with persistent PKA which activates transcriptional factors, creating proteins which cause increase insertion of receptors in the postsynaptic membrane and increase response to an incoming stimulus in the presynaptic neurone
if you block protein synthesis in aplysia you don’t get long term sensitisation but still get short term sensitisation

61
Q
A

PSC3008 (28 decks)

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