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PSYCH 371 > Chapter 3A: Synaptic Plasticity in Complex Systems, Long-Term Potentiation (LTP) > Flashcards

Chapter 3A: Synaptic Plasticity in Complex Systems, Long-Term Potentiation (LTP) Flashcards

1
Q

What is the Hebbian synapse?

A

based upon simple associative learning & memory principles, Donald Hebb came up with a theoretical mechanism of synaptic plasticity involving activity-dependent coincidence

“when an axon of cell A excites cell C and repeatedly or persistently takes part in firing it, some growth process or metabolic change takes place in one or both cells so that A’s efficiency in one or both cells so that A’s efficiency as one of the cells firing C is increased”

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2
Q

Do Hebbian synapses exist?

A

yes
activity dependent enhancement of synaptic transmission
LTP

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3
Q

What did Bliss and Lomo determine about long term potentiation?

A

study of the physiology of synaptic transmission in the hippocampus

high frequency stimulation of a particular fibre pathway produced a long-lasting physiological facilitation of its efficacy

called long-term potentiation (LTP)

immediately labeled as a potential model for the synaptic plasticity assumed to be involved in memory

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4
Q

What is the definition of long-term potentiation?

A

a long-lasting and activity-dependent increase in synaptic efficacy

synaptic facilitation

same inputs yields a bigger output

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5
Q

What is involved in the induction of long-term potentiation?

A

LTP due to coincidental activity in pre- and post-synaptic neurons

Hebbian mechanism

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6
Q

What is the presynaptic activity required in the induction of long-term potentiation?

A

neurotransmitter (glutamate) release

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7
Q

What is the postsynaptic activity required in the induction of long-term potentiation?

A

“threshold” depolarization

example: spiking

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8
Q

How is co-operativity a property of long-term potentiation?

A

LTP exhibits a threshold, that is it requires a given strength to stimulate

need to have something happen post-synaptically at great strength

probability of evoking LTP increases with the strength of stimulation and an increase in the number of fibres recruited during the stimulation

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9
Q

How is associativity a property of long-term potentiation?

A

LTP can be evoked by paired (coincidental) stimulation of two different inputs

by simultaneously activating two different pathways to the same target, one weakly and the other strongly, LTP can be induced in the weakly stimulated pathway

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10
Q

How is specificty a property of long-term potentiation?

A

LTP is expressed only in active (not inactive) synapses

LTP induced in an independent pathway does not spill over to other unstimulated pathways

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11
Q

What is the threshold for LTP?

A

strong activation of inputs is more likely to evoke LTP

simultaneous activation of many inputs
strong activation of single input

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12
Q

Why is temporal contiguity important to LTP?

A

pairing independent weak with strong stimuli

induces LTP in weak pathway
weak pathway sub-threshold
strong pathway supra-threshold

similar principle to cooperativity but non-anatomical overlap

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13
Q

Why is LTP only exhibited in active synapses?

A

supra-threshold stimulation to a given pathway enhances the response to ONLY that pathway

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14
Q

What is the main mechanism of LTP?

A

threshold stimuli release large amounts of glutamate onto two types of receptors:
AMPA receptors (classic ionotropic neurotransmission)
NMDA receptors (conditioned ionotropic neurotransmission, Ca2+ entry)

result: larger response recorded for same input

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15
Q

How does the release of glutamate onto NMDA receptors cause the activation of second messenger systems?

A

post synaptic: increase in receptor responsiveness
post synaptic: increase in receptor numbers
pre synaptic: increase neurotransmitter release

anatomical effects: increased synaptic contacts

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16
Q

Why is the NMDA receptor critical to LTP?

A

blockade eliminates induction of LTP

NMDA double gating provides LTP with the properties of specificity, cooperativity, and associativity

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17
Q

How is the NMDA receptor double gated?

A

double-gated – coincidence detector

ligand dependent (requires binding of neurotransmitter) as well as voltage-dependent (requires depolarization to remove Mg2+ block of channel pore)

activation requires both elements: glutamate binding and postsynaptic depolarization (via AMPA receptor activation and temporal and spatial summation of EPSPs)

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18
Q

What is the relationship between Ca2+ and LTP?

A

NMDA receptor channel permeable to Ca2+: depolarizes postsynaptic neuron, acts as second messenger

postsynaptic Ca2+ increases critical for LTP: Ca2+ chelators block LTP induction, release of caged Ca2+ induces LTP

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19
Q

Increases in intracellular Ca2+ activates which protein kinases?

A

CaMKII
PKC
MAPK
PKA and tyrosine kinase

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20
Q

What is the function of CAMKII in LTP?

A

activated by LTP-inducing stimuli

activation induces LTP

inhibition blocks LTP

21
Q

What is the function of PKC in LTP?

A

activated by LTP-inducing stimuli

activation induces LTP

inhibition blocks LTP

22
Q

What is the function of MAPK in LTP?

A

activated by phosphorylation processes during LTP or Ca2+ directly

inhibition blocks gene expression necessary for late LTP

23
Q

What is the function of PKA and tyrosine kinase in LTP?

A

specific for strong patterned activity

EC-DG synapse specific

24
Q

What is the time course of LTP?

A

LTP has been shown to last days and even weeks

25
Q

What is the early - induction phase of LTP?

A

NMDA receptor activation and calcium dependence

26
Q

What is the medium - expression phase of LTP?

A

changes to receptors and release machinery

local protein synthesis

27
Q

What is the late - maintenance phase of LTP?

A

genomic involvement, transcription dependent

anatomical changes?

28
Q

What is the definition of long-term depression?

A

a long-lasting and activity-dependent decrease in synaptic efficacy

synaptic depression

same input yields a smaller output

29
Q

What does presynaptic activity without postsynaptic activity have to do with LTD?

A

weak, low frequency repetitive stimulation of input fibers alone

explicit unpairing of weak stimulation and strong stimulation of input fibres (weak input shows LTD)

30
Q

What does postsynaptic activity without presynaptic activity have to do with LTD?

A

strong, low frequency repetitive depolarization of postsynaptic cell alone

explicit unpairing of postsynaptic cell depolarization with weak stimulation of input fibres

31
Q

What is the mechanism of LTD?

A

likely both pre and post-synaptic elements: decrease in neurotransmitter release, decrease in receptor numbers

due to a weak (subthreshold for LTP) elevation of postsynaptic Ca2+: activation of phosphatases (reduction of kinase activity)

32
Q

What is the purpose the mechanisms of LTD?

A

desaturation of synapses

contrast effects between potentiated and unpotentiated synapses

33
Q

How are LTP and LTD generalized brain phenomena?

A

although LTP and LTD were discovered and extensively studied in the hippocampus, both phenomena have been described in many other brain areas including:
neocortex
cerebellum
subcortical structures; e.g. amygdala
brainstem
spinal cord

34
Q

What are the similarities of LTP to learning and memory?

A

LTP: activity-dependent, cooperative, associative, input specific, time course (rapid induction, long duration, temporal phases: early and late)

Learning and memory: experience-dependent, attention-dependent, associative, stimulus specific, time course (rapid induction, long duration, temporal phases: short-term and long-term)

35
Q

What would be true if LTP is a neural analogue of learning and memory?

A

learning should elicit an LTP-like change in the brain

disruption or blockade of LTP should disrupt or prevent learning but should not interfere with previous memories

artificial LTP should interfere with previous memories

artificial LTP should interfere with normal learning or induce false memories, learning should also “saturate” LTP

reversal of LTP should erase previous memories

36
Q

What are some questions about the correlation between LTP and learning/memory?

A

does the ability to induce LTP relate to the ability to learn? (developmental or genetic modifications in LTP)

does learning “induce” an LTP like modification? (behavioral LTP)

37
Q

What are some questions about the perturbation between LTP and learning/memory?

A

does blocking LTP block learning and memory?

does inducing LTP by artificial means interfere with learning and memory?

38
Q

Is the ability to induce or sustain LTP correlated with learning and memory?

A

older rats have poor hippocampal LTP and show poor spatial memory

spatial memory in developing rats emerges at the same time that the hippocampus is functional and capable of LTP

different inbred strains of mice show differences in LTP

problem: not perfectly correlated with learning and memory performance

39
Q

Do the changes inherent in behavioral learning and memory induce LTP-like changes in the brain (behavioral LTP)?

A

“enriched” animals display LTP-like enhancements

fear conditioning commensurate with LTP-like enhancement of thalamic input to amygdala

motor learning yields differences in LTP abilities of motor cortex

40
Q

What is the behavioral LTP experiment involving conditioned fear and the amygdala?

A

condition: pair buzzer with electric shock, rats freeze when exposed to buzzer alone (fear response)

method: measure evoked potential in amygdala to thalamic input

result: LTP induced in pathway expressed as bigger potential to electrical AND auditory stimulation, fear learning results in bigger potential to electrical stimulation

41
Q

What was the behavioral LTP experiment involving motor learning?

A

condition: one hand reaching task

method: measure evoked potential in ipsilateral and contralateral motor cortex

result: bigger evoked potential in contralateral motor cortex following the training

42
Q

What was the behavioral LTP experiment involving enriched environments?

A

condition: rats housed in enriched environments

test: amplitude of hippocampal evoked potentials

result: bigger potentials in enriched rats

43
Q

Do alterations in the ability to induce or sustain LTP also alter learning and memory?

A

pharmacological, genetic: interfering with the process of LTP generally interferes with learning and memory

protein inhibitors differentially interfere with early versus late stages of LTP and memory: parallel elements of induction versus expression in LTP and memory

44
Q

Does behavioral learning and memory alter the ability of circuits to express LTP and vice versa?

A

in old rats, memory is impaired after the induction of LTP

saturation of LTP impairs learning ability

LTP like changes in motor cortex after motor learning also affect difficulty in eliciting experimental LTP

45
Q

What was the Morris water maze experiment involving hippocampal LTP and spatial memory?

A

condition: spatial learning in Morris water maze

method: intrahippocampal infusion of AP-5 (block LTP)

result: impairments in spatial learning, similar results with genetic modifications of LTP (CaMKII)

46
Q

What was the place cell experiment involving hippocampal LTP and spatial memory?

A

condition: open field foraging while recording multiple place cells in hippocampus

method: genetic modification of LTP (CaMKII)

result: place field instability, similar results with pharmacological blockade of LTP (AP-5)

47
Q

What are some examples of universal cellular and molecular mechanisms?

A

electrical events
2nd messenger systems
protein kinases
protein phosphorylation
gene expression
maintained electrophysiological changes

48
Q
A

PSYCH 371 (17 decks)

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