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BS42018- Mapping Memories in the Brain > BS42018 L3+4 > Flashcards

BS42018 L3+4 Flashcards

1
Q

what frequency (Hz) distinguishes between induction of LTD and LTP?

A

8Hz

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2
Q

what do different firing frequencies do regarding synaptic plasticity?

A

different firing frequencies will produce different levels of NMDAR activation
this dictates the level of intracellular calcium that enters the post-synaptic cell and also dictates whether you see persistent depression or LTP

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3
Q

what are the three temporal phases of LTP?

A
  1. Dependent on post-translational modification of existing protein- ie. Phosphorylation
  2. Dependent on synthesis of new protein from existing mRNA- ie. mRNA translation
  3. Dependent on synthesis of new protein and new mRNA- ie. Gene transcription, so involves the nucleus rather than the synapse perse
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4
Q

what are the timescales of the three temporal phases of LTP?

A

phosphorylation- occurs after first hour of stimulation
mRNA translation- occurs between hours 1-2
gene transcription- occurs 3+ hours after stimulation

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5
Q

how can you inhibit the early phase of LTP?

A

by inhibiting a variety of kinases that have shown to phosphorylate proteins at the synapse
these include- PKA, PKC, PKG, ERL, CAMKII, PYK2, Fyn

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6
Q

what does activation of Ca2+ dependent kinases do?

A

induce LTP

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7
Q

what does activation of phosphatases do?

A

induce LTD

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8
Q

give examples of approaches used to identify protein involvement or specific targets in LTP (4)

A
  • receptor antagonists
  • enzyme inhibitors
  • knockout mice
  • use of inactive/dominant negative forms
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9
Q

give a specific example of a knockout model used to investigate protein involvement in LTP

A

CAMKII a-subunit knockout mouse

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10
Q

what did the CAMKII a-subunit knockout model show?

A

not only CAMKII is involved as there was still amplitude

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11
Q

what are the mechanisms for the maintenance of early phase synaptic plasticity?

A

phosphorylation of receptors

receptor trafficking

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12
Q

which serine residue is down regulated after LTD in GluA1 subunits?

A

S845

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13
Q

what happens to ser831 after LTP in GluA1 subunits?

A

the level of phosphorylation is upregulated

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14
Q

under resting conditions what are the states of s845 and s831?

A

s845 is phosphorylated

s831 is dephosphorylated

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15
Q

what functional effects does LTP have on AMPARs?

A

increased conductance and increased trafficking to membrane

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16
Q

what is the evidence that GluA receptors traffic during LTP?

A

indirect- from studies that block post-synaptic interactions with regulatory/trafficking proteins eg PICK/GRIP etc. also evidence from silent synapses.
Direct- from immunohistochemical detection of surface GluA receptors (culture) and from imaging fluorescent GluA chimeras (eg. SEP-GluA1).

17
Q

why is phosphorylation not a sufficient long term LTP solution?

A

it is heavily reliant on being driven by kinase and phosphorylation of AMPA receptors and most kinases don’t function long term enough to be able to drive changes that are able to last for weeks or months.

18
Q

where is the mRNA involved in phase II of synaptic plasticity (mRNA/local protein synthesis) likely to be located?

A

in the dendrites to maintain synaptic specificity of plasticity

19
Q

where is the mRNA involved in phase II of synaptic plasticity (mRNA/local protein synthesis) likely to be located?

A

in the dendrites to maintain synaptic specificity of plasticity

20
Q

stimulation of protein synthesis from mRNAs could involve; (3)

A
  • Inhibition of mRNA degradation, leading to elevated mRNA levels (observed), and increased synthesis of the corresponding protein (if the mRNA levels are rate-limiting).
  • Phosphorylation of ribosomal proteins near the synapse (observed), leading to more efficient translation of the mRNA.
  • Phosphorylation of ribosomal proteins is triggered by ERK.
21
Q

how would you alter the number of glutamate receptors on the post synaptic membrane?

A

Phase 1; increase protein delivery, membrane insertion/trafficking and via lateral mobility
Phase 2 and 3; increase protein synthesis, local protein synthesis and somatic synthesis (general protein trafficking).

22
Q

gene transcription is activated by transcription factors. what types of TFs are there?

A

constitutive TFs, inducible TFs.

23
Q

give examples of constitutive and inducible TFs

A

constitutive- CREB, Elk1, NFkappaB

inducible- egr1, junB?

24
Q

what happens rapidly after triggering of synaptic plasticity?

A

morphological changes

25
Q

what evidence is there for the mobility of receptors at the synapse? (4)

A
  • use of MK-801 (NMDAR)
  • confocal imaging/ two-photon imaging
  • quantum dots
  • observing cultures
26
Q

what is the evidence for local protein synthesis in phase 2 of LTP?

A

Vickers in 2005 used whole cell recordings to examine LTP in 1) dendrites still attached to the nucleus and 2) dendrites that had been cut off from the nucleus.

cycloheximide was then administered and in both cases LTP was blocked after an hour.

this suggests that the block occurred in phase 2 and did not require the nuclear component- it is occurring at the dendritic level.

27
Q

how does synthesis of new protein and new mRNA come about in phase 3 of LTP?

A

gene transcription is activated by transcription factors

28
Q

highly specific involvement of PKA is essential in which stage of LTP?

A

stage 3

29
Q

How are IEGs involved in LTP? (6)

A
  • Ca2+ activates kinase which results in short term effects.
  • Kinase also enters nucleus
  • Causes phosphorylation of a transcription factor
  • Binds to IEG DNA and initiates transcription (or alternatively phosphorylation of a repressor protein, eg EF-2, initiates transcription).
  • IEG product (eg. FOS) is itself a transcription factor
  • Initiates synthesis of other proteins.
30
Q

what is the evidence that shows zif268 is required for expression of late-LTP and long term memories?

A

ZIF knockout mouse line- shows no deficits in early LTP but up to 4 days after LTP induction you start to see deficits in LTP process. they also show correlated deficits in Morris water maze.

31
Q

what is anterograde alteration?

A

interventions that prevent or limit the induction of synaptic weight changes during a learning experience should block or impair the animal’s memory of that experience.
(Interventions enhancing plasticity might also improve learning?)

32
Q

what experiment is often used to assess anterograde alteration?

A

Morris Water maze

BS42018- Mapping Memories in the Brain (4 decks)

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