Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Neuroscience 1: cells and circuits > Synaptic plasticity > Flashcards

Synaptic plasticity Flashcards

1
Q

What are some autoimmune synapse diseases?

A

Lambert Eaton myastenic disease, myasthenia gravis and anti NMDA-R encephalitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What are the quantal content, and what is it dependent on?

A

The mean number of vesicles released pr AP = the number of release sites (N) x the probability of release (P)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What are the mean synaptic current dependent on (give the equation)?

A

I = NPQ
N: number of release sites
P: probability of SV release
Q: quantal size (postsynaptic response pr SV)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

How are P (probability of SV release) estimated?

A

By varying the extracellular [Ca2+] in an experiment

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What is the pool of vesicles ready for SV release called?

A

The readily releasable pool (RRP)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What are the definition of short-term synaptic plasticity?

A

Changes in synaptic strength due to rapid stimulation, which are readily reversable when stim stops (only lasts for a few minutes or less)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What types of STP are there?

A

Depression, facilitation, potentiation and augmentation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What is the difference augmentation and potentiation?

A

Both enhances the ability of incoming Ca2+ to trigger fusion of vesicles, but in different time scales:
- augmentation: within a few secs
- potentiation: within 10s of secs or mins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Describe depression vs facilitation.

A

Depression: depletion of RRP
Facilitation: increase release probability

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Describe the meachanism of depression on the pre- vs postsynaptic side

A

Pre: mediated bt changes in N, e.g., depletion of RRP vesicles, slow refilling in the pool
Post: mediated by changes in Q, e.g., receptor density or receptor saturation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Describe the meachanism of potentiation on the presynaptic side

A

Pre: mediated bt changes in P, e.g., longer AP trains aka tonic synapses

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What is the residual Ca2+ hypothesis?

A

Stimulation frequency must be so fast that the residual Ca2+ has not subsided, requires fast refilling of RRP and the assumption that this mechanism is Ca2+ dependent

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What does augmentation, facillitation and potentiation all depend on?

A

Intracellular [Ca2+]

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What characterizes a depressing synapse?

A

High release probability, RRP siza is large at rest, refilling of RRP is relatively slow, RRP size decreases upon stim

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What characterizes a facilitating synapse?

A

Low release probability, RRP size is small at rest, refilling of RRP are Ca2+ dependent and very fast, RRP size increase upon stim

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Are depression and facilitation present in the same synapses?

A

Yes (it seems), many synapses display transient facilitation and persistent depression

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What are the roles of STP?

A

Depression: “low pass” filter, info about start of stim
Facilitation: “high pass” filter, info about persistence of stim

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What are the molecular mechanism behind STP, and what proteins are involved?

A

Vesicle priming:
- Munc13:
Munc13A –> tight coupling –> depression
Munc13B –> loose coupling –> facilitation
- Synaptotagmin: facilitation sensor (syn7 has a higher Ca2+ affinity –> binds to residual Ca2+ –> facilitation)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What is the definition of LTP?

A

The strength of synapses between neurons in the CNS is potentiated for prolonged periods following brief but intense synaptic activation

20
Q

How does spaced repitition affect short term memory?

A

Converting it into long term

21
Q

What are habituation?

A

A decrease in effectiveness of a stimulus in creating a response following repeated exposure to the stimulus

22
Q

What are sensitization?

A

An increase in sensitivity/response to a stimulus following repeated exposure a strong/painfull stimulus

23
Q

What are the molecular mechanism behind LT sensitization?

A

PKA recruit MAPK + CREB –> gene transcription

24
Q

What are the molecular mechanism behing ST sensitization?

A

PKA inhibits K+ channels –> stronger depol and Ca2+ influx

25
Q

How does spatial training affect the hippocampus?

A

Gray matter increase

26
Q

Where are the mechanism behind LTP, pre- or post?

A

Postsynaptic

27
Q

What is essential for LTP?

A

What fires together, wires together: the activity in the pre- and post synapse needto occur at the same time

28
Q

What is the difference between homo- and heterosynaptic transmission?

A

Homo: LTP is restricted to the input paired with the postsynaptic depol
Hetero: LTP can spread from activated synapses to nearby synapses that have not undergone the pairing procedure

29
Q

What is the mechanism behind heterosynaptic potentiation, and what does it possibly play a role in?

A

Ca2+ diffusing via NMDA-R activation
Possible role in associative learning

30
Q

What receptor activation does LTP rely on?

A

NMDA-R, as it is Ca2+ permeable

31
Q

What are NMDA-R activation dependent on?

A

AMPA-R activation: depol removes Mg2+ block from NMDA-R

32
Q

What is the induction of LTP due to?

A

Accumulation of postsynaptic Ca2+ - a brief increase (2.5s) after tetanic stim is sufficient

33
Q

What are spines?

A

Micron-sized protrusions along the dendritic shaft, that limit the diffusion of proteins and Ca2+ ions

34
Q

Describe the signaling pathway behind LTP.

A

Glutamate binds to and gates AMPA-R —> influx of Na+ —> depol. —> Mg2+ block in NMDA-R is removed —> NMDA-R is gated (glut. also binds here) —> influx of Na+ and Ca2+
—> Ca2+ activates CaMKII and PKC —> phosphorylation of AMPA-R
—> Ca2+ activates synaptotagmins —> insertion of new AMPA-R in the membrane

35
Q

What are LTP accompanied with?

A

Morphological changes in the postsynaptic membrane: spines

36
Q

What are the difinition of LTD?

A

A long lasting decrease in the efficiency of synaptic transmission mediated by the synaptic activation of AMPA-Rs

37
Q

What receptors are essential for LTD?

A

Also NMDA-Rs, as the slow and small increase in [Ca2+] here activates phosphatases –> internalization of AMPA-Rs

38
Q

How are the spike-timing dependent plasticity in LTP vs LTD?

A

LTP: postsynaptic AP comes after pre AP
LTD: post AP comes before pre AP

39
Q

What are the role of astrocytes in synaptic plasticity?

A

Release D-serine which are a co-ligand of NMDA-R

40
Q

What disease is thought to be a plasticity disease?

A

Alzheimers

41
Q

What are some mutation/genetic synapse diseases?

A

ADHD, schizophrenia, epilepsy etc.

42
Q

How are AD a plasticity disease?

A

Blocking axonal transport –> LTP is no longer lasting

43
Q

What types of synapse diseases are there?

A

Protein misfolding, plasticity, autoimmune, mutations/genetic leading to disruption of either the pre- or postsynaptic machinery

44
Q

How does synaptic genes differ from average genes?

A

They are longer, and therefore more suceptible for mutation

45
Q

What are diseases caused by malfunction in the SNARE complex called? Mention one.

A

SNARopathies
Epilepsy

Neuroscience 1: cells and circuits (42 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions