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Synpatic Plasticity > Synaptic Plasticity > Flashcards

Synaptic Plasticity Flashcards

1
Q

Name the 3 distinct temporal phases of LTP?

A
  1. Dependent on post-translational modification of existing proteins.
  2. Dependent on synthesis of new protein from existing mRNA.
  3. Dependent on synthesis of new protein.
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2
Q

How long does phase 1 of the temporal phase last?

A

0-1hr.

Covalent modification of existing synaptic proteins.

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3
Q

How long does phase 2 of the temporal phase last?

A

1-2 hrs.

The translation of pre-existing mRNAs.

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4
Q

How long does phase 3 of the temporal phase last?

A

3hrs+

Gene induction, transcription and translation.

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5
Q

Name the 8 types of kinases that inhibit early phase LTP?

A
  1. PKA
  2. PKC
  3. PKG
  4. ERK
  5. CamK11
  6. CamKIV
  7. PYK2
  8. Fyn
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6
Q

Is it single or multiple pathways that determine the plasticity response?

A

Multiple parallel pathways

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7
Q

How do NMDAR mediate LTP and LTD?

A

By mediating calcium rise and thus engage kinases and phosphatases.

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8
Q

Name the 4 ways to test that proteins are involved in synaptic plasticity?

A
  1. Receptor antagonists.
  2. Enzyme inhibitors.
  3. Knockout mice.
  4. Use of inactives.
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9
Q

Role of CAMK11?

A

Has a role in LTP.

Blocked by APV.

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10
Q

Name the two mechanisms for maintenance of early phase synaptic plasticity?

A
  1. Phosphorylation of receptors.

2. Receptor trafficking

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11
Q

What state of the glutamate receptor is associated with LTP and LTD?

A

Phosphorylation state.

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12
Q

How many units make up glutamate receptors?

A

Heteromers.

4 subunits. Many composed of GluA1 and 2

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13
Q

What part of the GluA1 has to be phospohrylated to effect trafficking?

A

s831 and S845

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14
Q

Phosphorylation of s831 of GluA1 effects?

A

LTP

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15
Q

Dephosphorylation of ser845 of GluA1 effects?

A

LTD

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16
Q

Low freq stimulation causes?

A

LTD

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17
Q

High freq stimulation causes?

A

LTP

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18
Q

The pathway of LTP?

A 
Strong activity
High calcium
Phosphorylation
Increased conductance
Increased AMPAR number.
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19
Q

The pathway of LTD?

A 
Lower, sustained activity.
Moderate calcium
Dephosphorylation
Decreased conductance
Decreased AMPAR number
20
Q

Indirect evidence that GluAR traffic during LTP?

A

Block post-synpatic interactions.

21
Q

Direct evidence that GluAR traffic during LTP?

A

Immunohistochemical detection of surface GluA receptors.

22
Q

What does TARPs do?

A

Control AMPA receptor trafficking

Modulate the electrophysiological properties of AMPARs

23
Q

What happens to the AMPAR that lack GluA2

A

Shows inward rectification due to blocking of the channel by polyamines

24
Q

Name the 3 ways to increase postsynaptic receptor number?

A
  1. Increase of receptor delivery
  2. Lateral diffusion
  3. Removal of receptor.
25
Q

Are NMDA mobile?

A

Yes.

Can be inserted into the membrane.

26
Q

What are quantum dots (Qdots)?

A 
Semiconductor noncrystals. Water soluble and can be used in biological applications.
Have superior brightness.
Larger absorption cross section
More photostable.
Can monitor lateral diffusion.
27
Q

Describe the receptor trafficking model

A

See figure 1

28
Q

Describe the molecular basis of late phase LTM?

A

Phosphorylation is involved by not a long term mechanism.

PKM zeta or new proteins constantly being made.

29
Q

Describe what is involved in the phase 2 of synaptic plasticity?

A

Involve mRNA present in dendrites.

30
Q

What genes encode the mRNA in phase 2 of synaptic plasticity?

A

MAP2

CamKII

31
Q

name the 3 processes that are involved in protein synthesis from mRNAs in phase 2 synaptic plasticity?

A
  1. Inhibition of mRNA degradation
  2. Phosphorylation of ribosomal proteins.
  3. Phosphorylation triggered by ERK
32
Q

How would you alter glutamate receptor number in phase 1?

A

Increase protein delivery

Membrane insertion

33
Q

How would you alter glutamate receptor number in phase 2 and 3?

A

Increase protein synthesis

34
Q

Describe phase 2 of synaptic plasticity?

A

Synthesis of new protein and new mRNA

35
Q

Describe the role transcription factors have in phase 3 synaptic plasticity?

A

Activates gene transcription.
Binds to specific target sites
Regulates transcription of target gene.

36
Q

Name the two types of transcription factors?

A
  1. Constitutive TFs- present in an inactive form in cytoplasm
  2. Inducible TFs- activated as target genes.
37
Q

Inducible TFs is concisdered a IEGs why?

A

Immediate-early gene.

Rapid transient transcription after a stimulus

38
Q

Name the 3 constitutive TFs involved in synaptic plasticity?

A
  1. CREB
  2. EIK1
  3. NFKappaB
39
Q

Name the 2 inducible TFs involved in synaptic plasticity?

A
  1. zif268

2. junB

40
Q

Define CREB activation?

A

binds to DNA sequence called CRE, therefore regulates transcription of downstream gene.

41
Q

How does L-LTP differ from E-LTP?

A

Requires PKA and distinct signalling pathways

42
Q

Name the 7 steps that IEGs is involved in LTP?

A
  1. calcium activated kinase.
  2. Enter nucleus
  3. Phosphorylation of transcription factor.
  4. Binds to DNA and initiates transcription
  5. Phosphorylation a repressor.
  6. IEG product is a transcription factor.
  7. Initiates synthesis of other protein.
43
Q

Name the 3 late-response genes? and which target them

A
  1. BDNF- CREB target.
  2. NCAM (neuronal cell adhesion molecule)- NFkB target.
  3. Proteasome genes and agrin- zif268 target.
44
Q

Describe the process of NMDA stimulating increase in AMPA?

A

Figure 2.

45
Q

Name the two types of morphological changes thought to occur during LTP?

A

Synapse splitting

Enlarged postsynaptic density.

46
Q

What is the role of neuromodulators and name the 6 of them?

A

Regulates synaptic plasticity.

Leptin, DA, 2AG, ACh, 5-HT and histamine.

Synpatic Plasticity (3 decks)

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