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BMSc - Synaptic Plasticity and Cognition > LTP > Flashcards

LTP Flashcards

1
Q

Define learning

A

The process of acquiring new information

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2
Q

Define memory

A

The persistence of learning
OR
The storage and retrieval of previously learned information

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3
Q

What are the two main forms of long term memory?

A

Declarative (knowing what)

Procedural (knowing how)

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4
Q

What is declarative memory split into?

A

Semantic

Episodic

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5
Q

What is synaptic plasticity?

A

A neurons ability to cause a persistent change in the synaptic strength

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6
Q

When does synaptic plasticity occur?

A

Development
Learning and memory
Ageing
Response to trauma and disease

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7
Q

Who discovered LTP?

A

Bliss and Lomo 1973

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8
Q

What are the 4 classical properties of LTP?

A

Persistence
Cooperativity
Associativity
Specificity

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9
Q

How did Bliss and Lomo discover LTP?

A

Repeated stimulation of the peforant path (same as the Schaffer collateral) they noted an increased response from the same level of stimulation

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10
Q

What is meant by “specificity” in LTP?

A

Specific to tetanised pathways

Non-tetanised inputs are not potentiated

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11
Q

What is meant by co-operativity?

A

There is an intensity threshold

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12
Q

What is meant by associativity?

A

Weak input will potentiate IF a strong convergent input is activated at the same time

(Classical conditioning)

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13
Q

What effect does classical conditioning have on synaptic strength?

A

If a weak conditioned stimulus causing firing at the same time as a strong unconditioned stimulus, there is increased synaptic strength of the weaker stimulus

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14
Q

What stimulation patterns can be used to induce LTP?

A

Tetanic stimulation (100Hz for 1 second, robust, not physiological)
Theta-burst stimulation (short burst @ 5 Hz, physiological)
Primed burst
Realistic stimulation

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15
Q

What are the main phases of LTP?

A

(Post-tetanic potentiation)
Early
Intermediate
Late

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16
Q

Which receptor types are vital for LTP?

A

NMDAR

even though AMPAR needed for immediate activation, NMDAR needed to carry the signal on

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17
Q

Outline what the 3 main stages of LTP are

A

1 - post-translational modifications
2 - mRNA translations
3 - protein synthesis and gene transcription

Use what u got whilst the rest is cookin

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18
Q

What occurs during the first phase of LTP?

A

AMPAR activation causes Ca2+ influx
Phosphorylates and activates membrane proteins
This recruits more AMPAR to the membrane

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19
Q

When does the early phase of LTP occur?

A

Within 1 hour of stimulation

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20
Q

What occurs during phase 2 of LTP?

A

Synthesis of new proteins from exsiting mRNA

Increased mRNA translation

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21
Q

When does phase 2 of LTP occur?

A

Within 3 hours of stimulation

22
Q

What occurs during stage 3 of LTP?

A

Gene transcription occurs to create new mRNA and synthesis new proteins

23
Q

When does phase 3 occur?

A

3 hours after stimulation

24
Q

How was LTP disocvered to be in 3 diff phases?

A

When given ansiomycin this blocks mRNA translation to protein the increased transmission increases for approx. half an hour then loss of activity and the fEPSP returned to baseline

When given actinomycin D, transcription is blocked, there was increased activity and sustained increase for up to 100 mins and then loss of activity and then return to baseline

(Draw this)

25
Q

Which group of enzymes are required for phase I LTP?

A

Kinases

26
Q

Which group of enzymes are required for LTD?

A

Phosphatases

27
Q

Phosphorylation of GluA1 at which position causes LTP?

A

ser831

28
Q

Phosphorylation of GluA2 at which position causes LTD?

A

ser845

29
Q

Outline the process of LTD

A 
Lower sustained activity 
Moderate calcium 
De phosphorylation 
Decreased conductance
Decreased AMPAR trafficking
30
Q

What evidence is there that GluA receptors traffic during LTP?

A

Immunohistochemical detection of surface GluA receptors and imaging of fluorescent tags show an increased number

31
Q

What are TARPs?

A

Transmembrane AMPAR regulatory proteins

32
Q

What is the role of TARPs?

A

Modulate AMPAR trafficking and lateral surface diffusion of AMPARs
Modulate biophysical properties of AMPARs

33
Q

What are the three main ways to increase post-synaptic receptor numbers?

A

Increase receptor delivery
Lateral diffusion
Reduce removal of receptor

34
Q

The mRNA for which kinases are present in dendrites?

A

MAP2

CamKII

35
Q

What is MAP2?

A

Microtubule-associated protein 2

Modulator of microtubules dynamics and growth

36
Q

What is CamKII?

A

A subunit involved in NMDAR-dependent signalling

37
Q

Which mechanisms may lead to increased protein synthesis in phase II?

A

Inhibition of mRNA degradation

Phosphorylation of ribosomal proteins triggered by ERK

38
Q

What activates gene transcription?

A

Transcription factors binding to specific target sites in the genome

Can either increase or decrease receptor function

39
Q

What are the two types of TF?

A

Constitutive

Inducible

40
Q

What is a constitutive TF?

A

Inactive and present in cytoplasm
Gets activated later

Eg CREB, Elk1, NFkappaB

41
Q

What is an inducible TF?

A

Activated by constituve TFs and then go on to transcribe their own target

Eg zif268, junB
(IEGs)

42
Q

How does CREB alter gene transcription?

A

Binds to cAMP response elements in the DNA which then dictate whether there is up or downregulation of transcription

43
Q

Outline the how IEGs are involved in LTP

A

Ca2+ actives kinases
Kinases enter nucleus to cause phosphorylation of TFs
IEGs bind to DNA to and induces transcription
GluRs created and AMPAR trafficked to the membrane

44
Q

How do we know that CaMKII is relevant to NMDAR signalling?

A

KO mice show much lower amplitude than WT

45
Q

What are the two mechanisms through which early synaptic plasticity is maintained?

A

Phosphorylation and trafficking of receptors

46
Q

How can lateral diffusion of receptors be observed?

A

With quantum dots

47
Q

Does zif268 induction cause LTP?

A

It is needed for late LTP

48
Q

Which late response genes are involved in LTP?

A

CREB targets: BDNF

NFkB targets: neuronal cell adhesion molecule (NCAM)

zif68 targets: proteasome genes, agrin

49
Q

What does NCAM do?

A

Promotes neurite outgrowth and maintenance of synaptic architecture

50
Q

What does persistence mean in terms of LTP?

A

Memory outlasts the induction of LTP

BMSc - Synaptic Plasticity and Cognition (5 decks)

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