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Developmental Neurobiology > lec 14-16. axon-target interactions > Flashcards

lec 14-16. axon-target interactions Flashcards

1
Q

trophic factors

A

“food” molecules that allow neurons to develop

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2
Q

neurotrophic factor hypothesis

A

1) neurons are produced in excess and then eliminated
2) targets release neurotrophic to promote survival, according to tissue size

effectively size control -> keeps tissue size and innervation proportional

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3
Q

how are excess axons eliminated

A

through cell death

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4
Q

cell death proteins and c. elegans homologues

A

Bcl-2: non-apoptotic (ced9)
Ced-3/4: pro-apoptotic (caspase1/ced4)
Bax
caspase 1/9

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5
Q

two types of caspases

A

caspase 9 - initiator

caspase 1 - executioner

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6
Q

nerve growth factor (NGF)

A

a type of neurotrophin dimer with active subunit B-NGF. affects cell survival, neurite survival, and even guides growth cones. binds to recetoprs and is internalised and transported to soma (DRG cell bodies also take up TrkA receptor)

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7
Q

TrkA receptor

A

high affinity receptor for NGF

tyrosine kinase receptor that forms signalling endosome and is transported throughout the cell

works by activating MAP kinase pathway (affecting proliferation) and Akt pathway (inhibits apoptosis)

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8
Q

p75-NTR

A

low affinity receptor for NGF, and also pro-NGF

can promote either cell survival or cell death based on the context (balance between ligand and receptor)

has intracellular death domain which initiates caspase mediated cell death in the absence of a ligand, and is thus a “dependence receptor”

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9
Q

neurotrophin family

A
  • brain-derived neurotrophic factors (BDNFs)
  • NT3
  • NT4/5

all are also dimers

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10
Q

examples of how different neurons are dependent on different neurotrophins

A 
nodose - BDNF, NT3
DRGs - BDNF, NTF, NGF
sympathetics - NT3, NGF
ruffini afferents - BDNF
Merkel - NT3, NGF, p75
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11
Q

how dependency of neurotrophins change with time

A

they initially have no dependency, then during development need NT3 and BDNF to reach target, then once at target need NGF and MSP

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12
Q

other families that neurotrophic factors belong to

A
  • glial-derived neutrotrophic factors

- cytokines (CNTF, HGF, MSP)

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13
Q

pruning

A

prune back excess axons, common in development and shares features such as cell fragmentation and phagocytosis with cell death

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14
Q

two examples of pruning

A

1) cortio-spinal and cortico-collicular initially start the same
2) can separate cell body and axon so axon is NGF-deprived so it starts shedding caspase 6 which binds to death receptor 6 and causes axon degradation

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15
Q

death receptor 6

A

a tumour necrosis factor with an intracellular death domain and causes cell death (or axon degradation) upon binding of ligand. therefore a “death receptor”

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16
Q

morphological changes that occur when growth cone turns into pre-synapse

A

1) filopodia retraction
2) membrane proteins + extracellular glycoproteins added
3) presynaptic vesicles, dense ECM, PSD, and receptors accumulate in the cleft

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17
Q

contacts by which neuron areas can initiate synapses?

A

growth cones mainly

but also axon branches, and dendritic filopodia

18
Q

when does synaptogenesis occur in spinal cord vs. cortex?

A

spinal cord and brainstem occurs pre-birth

cortex synapse form after birth

19
Q

Neurexins and Neuroligins

A

highly specific synapse CAMs that function in synapse specification (selecting appropriate contact), induction (clustering), and axon guidance

20
Q

intracellular domains of neurexins and neuroligins can..

A

assemble parts into active zone and post synaptic density

21
Q

spatial segregation of excitatory and inhibitory inputs

A

neurexins and neuroligins allow pre-synaptic cells to make contacts with multiple different post-synaptic partners

post-synaptic cells localise neuroligins which allows excitatory and inhibitory innervation by pre-synaptic cells to be separated

single neurons get multiple inputs and synapses are plastic and can be rearranged

22
Q

3 models for synapse/spine formation

A

1) dendritic spines develop independently of pre-synaptic inputs and dictate where these will be
2) pre-synaptic inputs induce spine formation
3) dendritic filopodia induce synapses in axons that are growing past

23
Q

how are contacts between dendrites and axons mediated?

A

they are directly mediated by CAMs (eg. neurexins/neuroligins) or through soluble factors released by either pre/post-synaptic cell

24
Q

CASK and PSD-95

A

contact triggers calcium influx which recruits cask (pre-synaptic) and PSD-95 (post-synaptic) which are scaffolding proteins that provide the framework for protein complexes in the active zone and pre-synaptic density

25
Q

stages of receptor clustering in neuromuscular junction

A

1) AChRs mRNA is expressed at low levels and channels are distributed
2) Agrin binds to MuSK which recruits Rapsyn which directly recruits AChRs
3) Neuregulin induces AChR expression in synaptic nuclei
4) Ach is released and can activate AChR anywhere, BUT if there is no agrin, its inhibits and destabalizes extra-synaptic AChRs

26
Q

TTX

A

a neurotoxin that block activity in neurons and leads to synapse loss

27
Q

survival of neurons depends on

A

coordinated electrical activity between pre and post synaptic cells

28
Q

proBDNF and p75-NTR

A

proBDNF binds to p75-NTR and triggers depression and retraction of axons

29
Q

BDNF and TrkB

A

BDNF binds to TrkB and triggers potentiation

30
Q

MMP

A

when there is coordinated electrical activity between two cells, it increases MMP activity which processes proBDNF to BDNF to strengthen the synapse through TrkB maturation

31
Q

ocular dominance columns

A

inputs from the LGN are segregated into eye-specific columns in layer 4 of the visual cortex. these columns reflect which eye/input is dominant. labelling only becomes apparent after eye opening

32
Q

long term potentiation

A

high frequency stimulation of a hippocampal synapse results in increased post-synaptic EPSP

33
Q

long term depression

A

low frequency stimulation of a hippocampal synapse results in decreased post-synaptic EPSP

34
Q

why NMDAr is a coincidence receptor

A

because first AMPAr need to be activated by glutamate to release Na+ and cause depolarisation which removes block from NMDA so it can allow Ca+ influx

so it is activated by pre-synaptic glutamate release and a post-synaptic action potential

35
Q

3 mechanisms operating in potentiation

A

1) changes in density and responsiveness to AMPAr -> increasing LTP and LTD
2) increase in synaptic size
3) changes in neurotransmitter release due to retrograde signals (NO, BDNF)

36
Q

development of neurotransmitter phenotypes

A

in early patterning phenotypes, a set of transcription factors are turned on which dictate the types of neurons progenitors give rise to and these same TFs stay on to dictate the set of neurotransmitters expressed

37
Q

motor neurons in triceps and pectoralis muscles have ___ inputs by ____

A

motor neurons in triceps and pectoralis muscles have monosynaptic inputs by proprioceptive Ia sensory neurons

38
Q

motor neurons in cutaneous max and latissimus dorsi have ___ inputs by ___ due to ____

A

motor neurons in cutaneous max and latissimus dorsi have polysynaptic inputs by interneurons due to muscles releasing GDNF which turns on Pea3 in motor neurons

39
Q

Er81

A

muscles expressing NT3 induce proprioceptive Ia sensory neurons to express Er81 which is required to develop central projection

40
Q

examples of dependent and independent targets

A

dependent: muscle spindles need sensory input to differentiate
independent: merkel discs are present before sensory innervation

41
Q

examples of how neurons can change as targets mature

A
  • early action potentials are produced by Ca+

- responses can also change from excitatory to inhibitory (GABAr switches from outward Cl- to inward Cl-)

Developmental Neurobiology (12 decks)

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