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Neuroscience > Synaptic Plasticity > Flashcards

Synaptic Plasticity Flashcards

1
Q

Evidence of depression following enhancement

A

PSP generation at high, medium and low calcium concentrations

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2
Q

Where are Munc13 and synaptotagmin involved

A

Synaptotagmin: prepares vesicular release- involved in Facilitation

Munc13-1: depression
Munc13-2: augmentation/potentiation

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3
Q

Munc13-1 role evidence

A

Munc13-1 KO evidence
Reduced depression after EPSCs/ IPSCs generated

Knock in of Calmodulin-insensitive Munc13-1 in mice
Reduced vesicle recovery time (presynaptic membrane capacitance and AMPAr mediated EPSCs)
Slower recovery from depression
Is a similar response to CaM inhibition in KOs

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4
Q

Munc13-2 role evidence

A

Munc13-2 KO
Reduced ability to induce augmentation
Rescue restored some augmentation

Mutant CaM insensitive 13-2 (W387R)
-Showed no augmentation

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5
Q

Calcium-sensitive domains of P/Q channels: role

A

IM Domain: facilitation and potentiation

CBD Domain: Depression

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6
Q

IM domain role evidence

A

Mutated IM domain shows reduced induction of facilitation and potentiation
-At low calcium levels, Ca2+ interacts with IM to induce P/Q channel activity

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7
Q

CBD domain role evidence

A

Mutated CBD domain shows no induction of depression

  • At high calcium levels, Ca2+ interacts with CBD to reduce P/Q channel activity
  • Not limited by vesicle release upon HFS
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8
Q

Theory of multiple mechanisms of Short term plasticity (Cheng 2008)

A

Deletion of both Calcium sensitive domains still leaves some enhancement and depression
There may be other factors which contribute to control

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9
Q

Hippocampal model of plasticity

A

Prolonged stimulation of perforant path

  • Elevated EPSP production in CA1 maintained for 3 hours
  • NMDA antagonist APV blocked
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10
Q

NMDA independent LTP in Hippocampal mossy fibres

A 
Mossy fibres (Dentate gyrus granule cells project to CA3 pyramidal cells)
Lack NMDA receptors, glutamate acts upon mGluRs and Kainate receptors
Presynaptic calcium entry directly increases cAMP
R type channels may mediate this effect (blocking P/Q does nothing)
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11
Q

Synaptic enlargement over time

A

Spines increase in size, produce increased EPSPs

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12
Q

Changes in AMPA subunit expression

A

Induction: mGluR1 homomers
- Greater inward current- naturally blocked by polyamine

Over time: replaced by mGluR1/mGluR2 heteromers
- Greater outward current (mGluR2 prevents influx)

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13
Q

LTP in inhibitory synapses

A

HFS IPSPs generated
Calcium and NMDA dependent
Not GABA dependent

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14
Q

Nitric oxide as a second messenger and opioids

A

Inhibition of synthesis (L-NAME)
Stimulation of synthesis (SNAP)

Opioids prevent IPSC administration
Upstream of cGMP production (administration reduces this effect)

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15
Q

Nitric oxide in alzheimers disease

A

Early AD
Increased vesicle release (EPSPSs)
L-NAME abolishes late LTP and reduces pre-pulse facilitation

Late AD
NO forms reactive oxygen species which are implicated in AD, depleting vesicular pools/reserves and accelerating disease progression

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16
Q

mGluR dependent LTD

A

Presynaptic- mGluR2
Decreases cAMP, common in mossy fibres/cerebellum

Post-synaptic- mGluR2

17
Q

Endocannabinoid and downstream effects

A

Agonism (WIN) and Antagonism (AM251) of CB1 receptors

CB1: induces LTD by activating PKA/cAMP
Reduced mIPSCs when PKA antagonised
Targets RIM-alpha (synaptic release machinery)
RIM-A KO reduces inhibitory LTD production

18
Q

TRPV1 mediated LTD

A

Capsacin
Antagonism/ KOs reduced effect

Calcineurin dependent
-Blocked by Cyclosporin A

19
Q

12-S-HPETE role

A

Potential natural agonist of TRPV1

-KO/Antagonism

20
Q

Optogenetic fear pairing and memory

A

Shock paired with sound, also with optogenetic stimulation
Training reduces lever presses
Optogenetic LTD- increased lever presses (mice forget)
Optogenetic LTP- reduced lever presses (mice remember again)

21
Q

Anisomycin and Actinomycin

A

Asinomycin (protein synthesis inhibitor)
Prevents initial EPSP spike but is maintained

Actinomycin (mRNA synthesis inhibitor)
EPSP spike but not maintained

22
Q

Initiation factors role

A

Phosphorylation of eif21s1 by DHPG induces LTD

Mutation of phosphorylation site Ser-Ala prevents this

23
Q

Synaptic tagging theory

A

Staufen staining- colocalises mRNA with actin

24
Q

CREB action

A

Forskolin (cAMP agonist)
Western blot increased pCREB with KCl

Fear shock conditioning LaCZ (B-galactoside reporter)
Morris Water Maze KOs reduced performance

25
Q

BDNF and CREB

A

BDNF- growth of inhibitory synapses

Mutation of CREB binding site

  • reduced CREB/RNA Pol II binding
  • reduced mRNA and glut
  • less staining of GABAergic synapses/ colocalisation of markers (GAD65, VGAT)
26
Q

NFAT role

A

CaN activated

Dopamine agonist increases NFAT activity (Luciferase)
Nifedipine decreases NFAT activity (Luciferase)

Enhances GluR2 expression

  • Increased luciferase activity in constitutively active mutant
  • Increased AMPA current
  • mutant glur2 reduced activity
27
Q

Cocaine and NFAT

Other cocaine effects

A

Increased NFATc4 translocation in cocaine use (western blot)
Due to increased dopaminergic activation in striatum

Increases H3K9 methyltransferase expression- increased gene expression

28
Q

DNA methylation evidence

A

DNMT inhibitor (Zebularine)- reduced LTP

Fear conditioning- reduces PPI methylation
Inhibiting methylation (Zebularine) reduces fear conditioning response

Reelin methylation reduced in response to fear conditioning
Methylation in hippocampus reverts to baseline after 24h

29
Q

Histone acetylation evidence

A

Fear conditioned mice- increased acetylation (Western blot)

HDAC2 O/E Morris Watermaze test performance reduced, less LTP
HDAC2KO/ Inhibition (Trichostatin A)

30
Q

HDAC and alzheimers

A

APP overexpression model increased HDAC2
Sodium butyrate (inhibitor) restores function
Improved memory in WTs
P25 OE: HDAC2 KOs similar to WTs in Morris water maze/fear conditioning

31
Q

HDAC4

A

Class 2a HDAC
Represses genes (neurotransmission, AMPA receptor trafficking) involved in synaptic transmission
Mutation assc. with Bradydactyly Mental retardation; cerebellar and visual neurodegeneration

32
Q

Histone H2A.Z subunit exchange

A

Presence of H2A.Z subunit appears to negatively affect plasticity

  • Fear conditioning: reduced h2afz gene expression
  • Depletion of H2A.Z in rats using AAV improved fear conditioning
  • Restrictive effect on memory creation
33
Q

Histone methylation

A

H3K4 increases expression
H3K9 decreases expression

fear conditioning performance

Neuroscience (17 decks)

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