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Neuro M101B > Module 1 Lecture 6: Synaptogenesis > Flashcards

Module 1 Lecture 6: Synaptogenesis Flashcards

1
Q

starburst amacrine function

A

detecting direction of motion

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2
Q

characteristics of fly Dscam1isoforms

A
  • homophilic
  • 4 alternatively spliced exons; 3 are for the ectodomain
  • 19008 ectodomain isoforms possible
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3
Q

what happens if dendritic arborization neurons don’t have Dscam1

A

spread out process of dendritic arborization (da) neurons collapse and cross over

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4
Q

is Dscam1 splicing selective?

A

no, nearly random

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5
Q

how is the Dscam1 identity developed

A

each neuron expresses several to a few tens of different isoforms

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6
Q

what does homophilic binding result in in Dscam1

A

repulsion

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7
Q

how is self-avoidance designed in Dscam1

A

each neuron can only bind its own set of Dscam1 isoforms

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8
Q

what results from reduced Dscam1 diversity (by overexpressing 1 isoform)

A

2 different da neurons that normally ignore each other now avoid crossing

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9
Q

how is ectodomain diversity in vertebrate Protocadherin clusters achieved

A

through alternative transcription start sites (contrast to fly Dscam1)
- each isoform is homophilic

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10
Q

function of domains EC2 and EC3 in Protocadherin clusters

A

mediate the specificity of homophilic binding

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11
Q

similarities between Protocadherin EC1 and Dscam Ig2

A

domains have similar folds

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12
Q

the question of synaptic specificity

A

after having arrived at the correct target area and layer, how do neurons choose the correct synaptic partners from among many contact partners?

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13
Q

example of stringent specificity

A

C3 neurons in fly visual system contacts both Tm1 and Tm2 neurons but only makes synapses with Tm1

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14
Q

biased specificity example

A

an On-SAC in the mouse retina has similar amount of contact with N- and V- ooDSGCs but makes more synapses with the V-type

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15
Q

types of synaptic specificity

A

adhesion, repulsion, elimination, and subcellular localization

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16
Q

first hypothesis for synaptic specificity

A

sequential: partner choice, then synapse formation

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17
Q

second hypothesis for synaptic specificity

A

package deal: combination of same cell adhesion molecules on pre- and post-synaptic cell mediate both partner choice and synapse formation

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18
Q

third hypothesis for synaptic specificity

A

make, then break: non-specific (promiscuous) synapses selectively eliminated after partner choice is made

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19
Q

why are in vitro studies of neurons less relevant to in vivo studies

A

neurons are synapse-happy and synapse-willing; they will readily make synapses with most sticky surfaces

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20
Q

what happens after neurogenesis and neuronal migration

A

axon guidance and dendritic arborization

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21
Q

what happens after axon guidance and dendritic arborization

A

nascent synapse formation

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22
Q

what happens after nascent synapse formation

A

either mature synapses or synapse elimination

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23
Q

what happens after mature synapses form

A

synapse elimination

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24
Q

what happens after synapse elimination

A

nascent synapse formation

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25
Q

first action from nascent synapses

A

engaging trans-cellular SAM complexes
- eg FLRTs/Teneurins <–> Lphns

26
Q

second action from nascent synapses

A

pre- and postsynaptic intracellular signals

27
Q

third action from nascent synapses

A

initial synapse assembly

28
Q

first action from mature synapses

A

signaling via diverse trans-synaptic SAM complexes
- eg Neurexins <–> Nlgns and Cblns/GluDs

29
Q

second action from mature synapses

A

pre- and postsynaptic protein activation (eg CASK)

30
Q

third action from mature synapses

A

specification of synapse properties

31
Q

first action of synapse elimination

A

disassembly of SAM complexes

32
Q

second action of synapse elimination

A

pre- and postsynaptic disruption signals (unknown)

33
Q

third action of synapse elimination

A

synapse elimination

34
Q

what happens if you disrupt gene/process involved in earlier steps in synapse formation

A

will not get to synapse formation

35
Q

what happens if you disrupt a gene/process involved in later steps of synapse development

A

may look like synapse formation was affected

36
Q

what do axons from CA3 region of the hippocampus form synapses with

A

CA1 pyramidal neurons in two of three possible layers (stratum oriens and s. radiatum and not s. lacunosum-moleculare

37
Q

where are Lphn2 and Lphn3 targeted

A

to distinct and non-overlapping regions of the post-synaptic CA1 neuron dendrites

38
Q

what does Lphn3 mediated synapse formation require

A

simultaneous binding of two pre-synaptic cell surface molecules

39
Q

how is specificity of synapse formation achieved?

A

specific compartmentalization of Lphn3 and co-incidence detection of correct pre-synaptic axons

40
Q

what is Lphn3 necessary for

A
  • formation of subset of excitatory synapses in cultured hippocampal neurons
  • synapse formation in s. oriens and s. radiatum but not s. lacunosum-moleculare
  • CA1 excitation by the Schaffer collateral fibers
41
Q

what happens without Lph3

A
  • loss in excitatory post-synapses (spines)
  • in vivo hippocampal neuron excitatory synapse function compromised
  • number of pre-synaptic CA3 neurons (origin of Schaffer collaterals) drop significantly without Lphn3
42
Q

characteristic of Lphn3 4A mutatnt

A

cannot bind FLRT

43
Q

characteristic of delta Lec

A

cannot bind Teneurin

44
Q

can binding mutants rescue loss of excitatory synapses

A

no

45
Q

what does Lphn3 dependent synapse formation in cultured hippocampal neurons require

A

both teneurin binding and FLRT binding by Lphn3

46
Q

can binding mutants rescue loss of excitatory synapses

A

no

47
Q

what is necessary for excitatory synapse function

A

Lphn ability to bind both pre-synaptic partners

48
Q

what are Schaffer collaterals

A

axons from CA3

49
Q

under what conditions do Schaffer collaterals come through

A

where Lphn3 is expressed

50
Q

what happens where Lphn2 is expressed

A

axons from the entorhinal cortex come through (perforant pathway)

51
Q

significance of Lphn3 capable of binding both pre-synaptic partners

A

is sufficient to rescue CA1 excitation in response to Schaffer collateral stimulation

52
Q

can Lphn2 expression rescue Lphn3-loss dependent increase in CA1 excitation in response to Schaffer collateral stimulation

A

no

53
Q

is Lphn3 necessary for CA1 excitation in response to perforant pathway stimulation

A

no

54
Q

rabies virus function

A

spreads from post-synaptic to pre-synaptic neuron; used for retrograde tracing

55
Q

first step of rabies virus experiment

A

introduce Cre to delete Lphn3

56
Q

second step of rabies virus experiment

A

introduce rescue constructs (eg WT or mutant Lphn3)

57
Q

third step of rabies virus experiment

A

set up retrograde tracing with rabies virus, engineered to ‘jump’ only 1 synapse (replication-deficient) and to carry GFP for marking the infected pre-synaptic neurons

58
Q

end result of the rabies virus experiment

A

Cre (which deletes the Lpn3 cKO allele), GFP, mCherry (red)

59
Q

what do pre-synaptic neurons express in the rabies virus experiment

A

GFP

60
Q

what is not affected by loss of Lphn3

A

number of pre-synaptic entorhinal cortex neurons (perforant pathway)

61
Q

significance of post-synaptic expression of Lphn3 in CA1 neurons

A

necessary and sufficient to form synapses specifically with Schaffer collaterals from CA3 neurons

62
Q
A

Neuro M101B (6 decks)

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