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developmental final > synapse formation and elimination > Flashcards

synapse formation and elimination Flashcards

1
Q

when are the synaptic building blocks made?

A

many synaptic building are premade in both pre and postsynaptic neurons.

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2
Q

how fast is synapse formation

A

it is rapid but matures structurally and functionally over time.

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3
Q

what induces differentiation

A

contact. this is via intercellular and intracellular signaling events.

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4
Q

what are the steps of synapse formation

A

1) motor axon filopodia express neurotransmitters
2) myotubes uncouple to form single-celled units soon after axon contact.
3) a small nuber of transmitter receptors are homogeneously distributed on myotube surface.
4) endogenous transmitter released from growth cones is detected nerve stimulation elicits post synaptic response.
5) axon filopodia and transmitter receptors are localized to mature zone.
6) functional synapse is formed.
7) presynapse specializations form; mature morphology
8) vigorous activity

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5
Q

what happens to the terminal upon contact?

A

maturation including vesicles, active zone, and release machinery

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6
Q

what happens to the cleft upon contact?

A

maturation involving ECM

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7
Q

what happens to the postsynaptic differentiation upon contact?

A

receptor clustering, PSD, golgi apparatus, coated vesicles.

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8
Q

when does synaptogenesis occur?

A

until adulthood and then still at low levels.

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9
Q

what mediates neurotransmitter receptor clustering upon contact

A

agrin-MuSK-LRP4 signaling

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10
Q

agrin

A

secreted proteoglycan

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11
Q

LPR4

A

agrin receptor with binding sites for MuSK

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12
Q

MuSK

A

muscle specific kinase

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13
Q

Dok-7

A

interacts with MuSK, required for its activation

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14
Q

Tid1

A

activates AChR phosphorylation necessary for interaction with rapsyns

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15
Q

rapsyn

A

AChR scaffolds. can self-associate.

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16
Q

what mediates glutamate receptor clustering in the CNS

A

ephrin-ephB signaling

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17
Q

which neurexin-neuroligan complexes are for excitatory

A

NLGN1/3/4

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18
Q

which neurexin-neuroligan complexes are for inhibitory

A

NLGN2

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19
Q

what else causes glutamate receptor clustering

A

cadherin family

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20
Q

what causes GABAR and NMDAR clustering

A

BDNF-trkB

21
Q

GluR4 clustering

A

Pentraxins (Narp, NP-1, NRP)

22
Q

MAGUKs (excitatory): e.g. PSD-95, SAP-102, PSD-93, SAP97

Gephyrin (inhibitory)

A

Scaffolding molecules (rapsyn analogs)

23
Q

Molecular pathways regulating terminal differentiation

A

Trans-synapic neurexin-neuroligin signaling
NLGN-1 for excitatory and NLGN-2 for inhibitory synapses
Wnt-7a (a soluble factor) FGF22 (a soluble factor)

24
Q

what Cell adhesion molecules mediate the interaction for synapse differentiation

A

many are immunoglobulin domain-containing proteins.
SynCAMs: (brain-specific) Cadherin superfamily (Ca2+ dependent)
Nectin-afadin adhesion system

25
Q

what happens when a growth cone is near a target?

A

it slows down. contact-dependent mechanism

Growth cones travel fast in the absence of target cells

26
Q

what changes happen to growth cones when exposed to guidance factors?

A

Depolarized when exposed to Netrin-1 (chemoaFractant)

Hyperpolarized when exposed to Sema3A (chemorepellant)

27
Q

the decision to build a synapse occurs when

A

1) Target-specific growth cone slow down; contact-dependent mechanism
2) growth cones display dynamic changes in response to known axon guidance factors
3) Ca2+ level increase within seconds following target contact – contact-evoked increase in Ca2+
4) Ca2+ induces ac-n polymeriza-on and cytoskeleton reorganiza-on in growth cones, facilita-ng terminal differen-a-on
5) Ca2+, PKC, cAMP-PKA may act in tandem
6) A large family of adhesion molecules involved
7) Astrocytes

28
Q

EPSP and IPSP dura-ons decrease dras-cally during postnatal development

A

Mechanism: Receptor isoform transition - neonatal channel forms open longer
Plasma membrane transporters: expression increases during postnatal
May limit behavioral capabilies in young animals

29
Q

Func-onal matura-on of synapses: reliability and short-term plas-city

A

Higher variaOon and failure in young animals
MaturaOon depends on presynapOc release properOes and postsynapOc channels and receptors
Failure to summate depolarizaOon or inhibiOon in young animals
§ Can be synapse or connecOon specific § PotenOal mechanisms:
§ Wide APs in young; refractory period § Releasable pools not fully ready for rapid release § PostsynapOc receptors desensiOzaOon

30
Q

why is refinement of synaptic connections necessary?

A

at birth synapse connections are imprecise, immature, and not useful. they are added, stabilized, or eliminated. dependent on sensory experience/activity. time of refinement varies for synapses.

31
Q

what are the three major ways to refine

A

topography, convergence, posysynaptically

32
Q

how do we measure convergence

A

using electrophysiology or imaging

33
Q

what is the visual pathway

A

Eye-RGC-LGN (thalamus)-cortex (L4)

34
Q

does LGN patterning require visual experience

A

no. at embryonic stages branches are seen in inappropriate layers, but after birth they are segregated

35
Q

Eye-specific stripes in the visual cortex

A

LGN terminal segrega$on pa[erns in adult visual cortex, layer IV
Forms aXer eye opening – requires visual experience
Due to synapse elimina$on and axon retrac$on

36
Q

what is the normal visual system in the cortex look like?

A

Visual cortex neuron coding: individual neurons fire ac$on poten$als when visual s$muli delivered to the appropriate eye
Layer IV neurons – mostly monocular
Outside Layer IV: mostly binocular due to local projec$ons from neighbor cells
Ocular dominance column

37
Q

effects of monocular deprivation

A

Ocular dominance shifted

Suggesting visual experience required in maintaining this.

38
Q

Effects of binocular deprivation

A

Ocular dominance intact
Many neurons unresponsive to visual stimuli
Suggesting competition, not vision per se

39
Q

Effects of ar2ficial strabismus (extraocular muscle surgery to alter the alignment of the eyes)

A

Ocular dominance remains but binocular cells lost
Sugges$ng near simultaneous $ming of synap$c ac$vity is important in allowing inputs to
remain connected func$onally to cor$cal neurons.

40
Q

Strabismus mimics amblyopia in humans

A

a visual s$mulus ac$vates different por$ons on the two re$nas so that individual cor$cal neurons are not ac$vated by both eyes at the same $me

41
Q

The compe$$on hypothesis

A

differences between ac$vity levels in each pathway determines afferent survival/removal

42
Q

Influence of GABAergic inhibi2on: delimits cri2cal periods

A

Increases inhibitory transmission shiXs cri$cal period earlier
Decreasing inhibitory transmission delays cri$cal period

43
Q

Temporal requirement

A

Synchrony of two inputs blocks elimina$on

44
Q

Spa2al requirement

A

A short distance between contacts – sugges$ng postsynap$c targets plays ac$ve role

45
Q

what is the role of spontaneous activity

A

forms and maintains initial and unstable connections/maps

46
Q

what is the mechanism of synaptic elimination?

A

heterosynaptic depression
synapses can be weakened or eliminated by the ac2vity of neighboring connec2ons (the compe22on hypothesis) via common postsynap2c cells – “ac2vity is detrimental”

47
Q

what are the spatial and temporal requirements of heterosynaptic depression

A

Spa$al requirement: < 50 μm; territory

Timing requirement: not at the same $me - compe$$on

48
Q

what cell dictates depression

A

Postsynap2c cells dictate heterosynap2c depression

Retrograde signaling may be involved also to remove terminals

49
Q

what molecular mechanisms mediate synapse elimination

A

calcium signaling, complment, autophagy, MHC class I

developmental final (9 decks)

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