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Developmental Neurobiology 🧠 > Final Exam: Chapter 8 > Flashcards

Final Exam: Chapter 8 Flashcards

1
Q

Once axons reach target…

A

form junctions and synapse
growth cone differentiates
postsynaptic neurons develops specialized site

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2
Q

Who makes decision to stop growth and differentiate?

A

Shared between pre/post synaptic neurons

intracellular signals are important

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3
Q

_______ important for postsynaptic clustering of Ach R at NMJ

A

presynaptic signals

postsynaptic slower to commit

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4
Q

As it matures, postsynaptic density

A

increases

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5
Q

Cells push away from each other to receive synaptic contacts. Do they do this because they get bigger?

A

no more dendrites, all connective features take up volume

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6
Q

Stages of synapse formation

A

1) Recognize signal
2) membrane glycoprotein
3) tight junctions
4) immature synapse
5) mature synapse: with ECM

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7
Q

What do growth cones release to find target?

Why does it do this?

A

NT, not always the final one through

helps cell realize partner, helps post synaptic cell initiate synaptic changes

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8
Q

Experiment: Growth cone in FM4-64 dye, depolarize to take FM into vesicles, depolarize again to release

A

vesicle proteins? in GC filopodia, early presynaptic machinery

ex: synatophycin (phicin)

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9
Q

Experiment: stimulate growth cone with myoball (ball of muscle cells) nearby

A

Result: longer left together, increase frequency and amplitude, lots of quick changes

muscle cell contact ENHANCES electrical transmission

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10
Q

Inject Ca2+ sensitive dye on GC and put them in contact with…

1) GC (nothing, it’s just the GC)
2) muscle cell
3) neuron
4) muscle cell, but in a Ca2+ free solution

A

1) resting Ca2+
2) increase ca2+
3/4) no rise

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11
Q

Growth cone + calcium ionophor

A

super permeable membrane, collapses, meets target

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12
Q

increase calcium = ___ GC

A

round Growth cone

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13
Q

Once contact between GC and muscle cell, calcium levels

A

rise

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14
Q

Netrin-1

A

chemoattractant, GC depolarized

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15
Q

Sema-3A

A

chemorepellent, GC hyperpolarized

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16
Q

Ca2+ flow in GC filopodia when ___ occurs.

influx Ca2+ = _____ polymerization

A

pre/post synaptic contact

actin polymerization

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17
Q

______ provides adhesion during synapse between GC and postsynaptic muscle

A

NCAM

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18
Q

What happens to NMJ synapses of drosophilia Fas2 mutants?

A

Retraction

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19
Q

Hippocampus uses ____ linking thing

Also forms ____ which allows presynaptic side to envelope them and hold it together.

A

Cadherins

Dendrite spines

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20
Q

Block cadherin, block…

A

synapse formation

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21
Q

CAMS and synapse formation: order it goes together

A

Actin- alpha catenin- beta catenin- cadherins

actin-Afadin-Nectin, which keeps is locked in

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22
Q

Presynaptic proteins: quick to the game

A

53 min: + Basoon labeling (presynaptic marker)

75 min: 90% contact complete active zones

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23
Q

What labels postsynaptic side?

A

PSD-95. Use that and bassoon for pre to see that presynaptic side is faster.

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24
Q

Intracellular signaling promotes differentiation: How to pre/post synaptic sides stabilize

A

Pre: Post

1) Neurexin: neuroligin
2) FGFR2: FGF
3) Frizzeled: Wnt

This results in stabilization
Postsynaptic has ligands

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25
Q

What happens to alpha-Btx after innervation?

A

now clustered at synapse

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26
Q

Is innervation required for alpha-btx clusters?

Experiment: HB9 -/- mice

A

No! still have alpha-btx stains .

Moral: Ach receptors tend to be around the right areas, even if not necessarily the perfect match up

alpha-btx labels Ach receptors

27
Q

Target cell contact results in…

A

increase presynaptic NT release
cell adhesion
Ca2+ entry
Clustering in NMJ

28
Q

Is clustering of spinal motor neurons and Ach receptors dependent on acetylcholine? If not, then why do they cluster?

A

Not acetylcholine

Cluster due to contact

29
Q

What is the cluster signal?

A

Agrin (neuronal)

30
Q

Experiment: Cut axons to basal lamina and remove muscle

A

Result: new muscle cells will still cluster, meaning the cluster signal is in the synaptic cleft

31
Q

Argin binds to Lrp4 and MuSK-P, because ___ and ___ needed for clustering

A

MuSK and Actin

32
Q

Musk recruits __ and ___ as scaffolding proteins, needed for acetylcholine clustering

A

Doc7 and Tid1

33
Q

If musk doesn’t touch raspsyn (anchors postsynaptic side) or AChR what gets it to the right place?

A

MASC and RATL

34
Q

If you KO Musk…

A

lose clusters

35
Q

What was the point of the chick and rat experiment?

A

neural agrin is what causes clustering

36
Q

CNS: what helps with clusters of NMDA and AMPA

A

1) Ephrin B- Eph B (NMDA)
2) pentroxins (NARP) - AMPA-glutamate to GluR4
3) Neurotrophin- trk: BDNF response, GABA and NMDA clusters.

37
Q

KO ephrin

A

don’t get nice AMPA clusters

38
Q

Glutamate Receptor:
____ adaptor protein for NMDA R
_____ adaptor protein for AMPA

A

NARP

TARP

39
Q

Glutamate Receptor: NLGN

A

binds to gephyrin (NRXIN), activates GDP/GTP exchange factor: COLLYBISTIN, interacts with NLGN2

40
Q

GABA receptor: early on gephyrin is anchoring ____ to syanpse

A

alpha-2 Gaba R

41
Q

GABA receptor: radixin holds ____ extrasynaptically, but loss of radixin does not disrupt clustering

A

GABA5

42
Q

Experiment: muscles prelabeled with rhodaneuro-bunganexin.
1) MN added
2) no MN added
Then labeled with fluorescent antibody

A

Only antibody = new inserted

1) 60% new
2) 20% new

Shows presynaptic terminal causes receptors to come in

43
Q

Experiment: TXX cuff to bock Na+ so no AP

A

NO transmission

normally, AP –> Ca2+ –> CAMK2 –> myogenin which inhibits Ach R on neighbors

44
Q

myogen

A

transcription fact, inhibits AchR expression in non-synaptic nuclei. If ttx cuff, can’t stop expression

45
Q

The Ca2+ –> CAMK2 –> myogen activates…

A

acetyl outside synapse

46
Q

KO agrin = ________

Can this be saved?

A

no aggregation

Yes! if we KO acetylcholine too!

47
Q

Dispersion signal

A

acetylcholine, activates cdk5 to put receptors in vesicles and inhibits aggregation genes

48
Q

Since too many glutamate receptors is bad, activity limits glutamate receptors by…

A

internalizing AMPA

49
Q

How does activity internalize AMPA?

A

1) Arc transcribed, AMPA out membrane, pull in to destroy

2) UBe3A: marks Arc for destruction, prevents arc from getting all receptors out

50
Q

Duration of EPSP and IPSP _____ over time

A

declines, goes faster so you can respond to new stuff quickly

51
Q

ErbB receptors and neuregulin do what to acetylcholine receptors

A

Change that gamma to epsilon over the course of development

52
Q

Early AP are (more/less) Ca2+ dependent than later ones

A

more

53
Q

After switching channel subtypes, time it takes to open/close channels…

A

decreases

54
Q

What channels increase over development? Which decrease?

A

L and N

T decrease

55
Q

Young glycine vs. adult glycine

A

young: alpha-2, open long time
adult: alpha-1, short open times

56
Q

Young GABA vs. Adult GABA

A

alpha 5 replaced by alpha 1

shorter open times in adult

57
Q

Experiment: picrotoxin (blocks GABA)
CNQX: blocks AMPA

A

only EPSP from NMDA

younger have larger lasting EPSP

58
Q

Ion gradient in cells: Why is Cl- not inhibitory when influx at first? Why hyperpolarization that makes inhibitory?

A

1) Glia maintain extracellular environment

2) symporters/ion pumps at early stages not good at getting Cl- out so equilibrium is crazy

59
Q

BIC-GABA receptors antagonists:
(BIC: inhibits transmission)

8 days vs. 33 days

A

8 days: decrease Ca2+, depolarize

33 days: increase Ca2+, hyperpolarized

Why depolarize IPSP, elevated Cl- in cell, so Cl- outflow

60
Q

Changing ___ to ___ helps get that Cl- out of the cell.

A

NKCC1 –> KCC2

61
Q

______ causes super sensitivity of receptors

A

denervation/blockade

62
Q

_____ at NMJ controls transcription of receptor proteins

A

neuregulin

63
Q

Maturation changes:

A

1) receptor Number & subtype
2) ion channel conductance
3) GABA R mediates excitatory transmission in young developing neurons

Developmental Neurobiology 🧠 (11 decks)

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