Final Exam: Chapter 8 Flashcards

(63 cards)

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
What happens to alpha-Btx after innervation?
now clustered at synapse
26
Is innervation required for alpha-btx clusters? | Experiment: HB9 -/- mice
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
Target cell contact results in...
increase presynaptic NT release cell adhesion Ca2+ entry Clustering in NMJ
28
Is clustering of spinal motor neurons and Ach receptors dependent on acetylcholine? If not, then why do they cluster?
Not acetylcholine Cluster due to contact
29
What is the cluster signal?
Agrin (neuronal)
30
Experiment: Cut axons to basal lamina and remove muscle
Result: new muscle cells will still cluster, meaning the cluster signal is in the synaptic cleft
31
Argin binds to Lrp4 and MuSK-P, because ___ and ___ needed for clustering
MuSK and Actin
32
Musk recruits __ and ___ as scaffolding proteins, needed for acetylcholine clustering
Doc7 and Tid1
33
If musk doesn't touch raspsyn (anchors postsynaptic side) or AChR what gets it to the right place?
MASC and RATL
34
If you KO Musk...
lose clusters
35
What was the point of the chick and rat experiment?
neural agrin is what causes clustering
36
CNS: what helps with clusters of NMDA and AMPA
1) Ephrin B- Eph B (NMDA) 2) pentroxins (NARP) - AMPA-glutamate to GluR4 3) Neurotrophin- trk: BDNF response, GABA and NMDA clusters.
37
KO ephrin
don't get nice AMPA clusters
38
Glutamate Receptor: ____ adaptor protein for NMDA R _____ adaptor protein for AMPA
NARP TARP
39
Glutamate Receptor: NLGN
binds to gephyrin (NRXIN), activates GDP/GTP exchange factor: COLLYBISTIN, interacts with NLGN2
40
GABA receptor: early on gephyrin is anchoring ____ to syanpse
alpha-2 Gaba R
41
GABA receptor: radixin holds ____ extrasynaptically, but loss of radixin does not disrupt clustering
GABA5
42
Experiment: muscles prelabeled with rhodaneuro-bunganexin. 1) MN added 2) no MN added Then labeled with fluorescent antibody
Only antibody = new inserted 1) 60% new 2) 20% new Shows presynaptic terminal causes receptors to come in
43
Experiment: TXX cuff to bock Na+ so no AP
NO transmission normally, AP --> Ca2+ --> CAMK2 --> myogenin which inhibits Ach R on neighbors
44
myogen
transcription fact, inhibits AchR expression in non-synaptic nuclei. If ttx cuff, can't stop expression
45
The Ca2+ --> CAMK2 --> myogen activates...
acetyl outside synapse
46
KO agrin = ________ | Can this be saved?
no aggregation Yes! if we KO acetylcholine too!
47
Dispersion signal
acetylcholine, activates cdk5 to put receptors in vesicles and inhibits aggregation genes
48
Since too many glutamate receptors is bad, activity limits glutamate receptors by...
internalizing AMPA
49
How does activity internalize AMPA?
1) Arc transcribed, AMPA out membrane, pull in to destroy | 2) UBe3A: marks Arc for destruction, prevents arc from getting all receptors out
50
Duration of EPSP and IPSP _____ over time
declines, goes faster so you can respond to new stuff quickly
51
ErbB receptors and neuregulin do what to acetylcholine receptors
Change that gamma to epsilon over the course of development
52
Early AP are (more/less) Ca2+ dependent than later ones
more
53
After switching channel subtypes, time it takes to open/close channels...
decreases
54
What channels increase over development? Which decrease?
L and N | T decrease
55
Young glycine vs. adult glycine
young: alpha-2, open long time adult: alpha-1, short open times
56
Young GABA vs. Adult GABA
alpha 5 replaced by alpha 1 | shorter open times in adult
57
Experiment: picrotoxin (blocks GABA) CNQX: blocks AMPA
only EPSP from NMDA younger have larger lasting EPSP
58
Ion gradient in cells: Why is Cl- not inhibitory when influx at first? Why hyperpolarization that makes inhibitory?
1) Glia maintain extracellular environment | 2) symporters/ion pumps at early stages not good at getting Cl- out so equilibrium is crazy
59
BIC-GABA receptors antagonists: (BIC: inhibits transmission) 8 days vs. 33 days
8 days: decrease Ca2+, depolarize 33 days: increase Ca2+, hyperpolarized Why depolarize IPSP, elevated Cl- in cell, so Cl- outflow
60
Changing ___ to ___ helps get that Cl- out of the cell.
NKCC1 --> KCC2
61
______ causes super sensitivity of receptors
denervation/blockade
62
_____ at NMJ controls transcription of receptor proteins
neuregulin
63
Maturation changes:
1) receptor Number & subtype 2) ion channel conductance 3) GABA R mediates excitatory transmission in young developing neurons