Wiring a Nervous System Flashcards

(43 cards)

1
Q

guidepost cels

A

direct outgrowing axons and change their direction

==>alter intracellular signaling with growth cones

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2
Q

pioneer neurons

A

first to grow in uncharted territory

growth cones are active filopodia

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3
Q

follower neurons

A

much simpler growth cones (fewer filopodia)–>latch to pioneers trail and form fasicles

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4
Q

some pioneer neurons

A

are transitory–they die and are replaced by permanent neurons

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5
Q

path finding neurons

A

developming neurons that respond to growth cones (lamellipodia and filopodia)

when they reach target they differentiate into pre syn terminals

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6
Q

trophic molecules

A

support growth and survival

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7
Q

tropic molecules

A

guide

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8
Q

extracellular matrix proteins

A

laminin, collagen, fibronectin

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9
Q

function of emp

A

interact with integrins on axon

  • -regulate extend of adhesion of growth cones
  • -allow to extend and pull axons along with them
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10
Q

cell adhesion molecules are used for

A

pioneer and follower neurons

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11
Q

what are cell adhesion molecules

A

CAM
Ca-indep
–act as both ligand and R
-hemophilic and heterophilic interactions

promote adherence amongst axon processes

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12
Q

chemoattractants/chemorepellants

A
slit
ephrin
netrin
semaphorin
neurotrophin
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13
Q

receptors

A
roundabout
Eph
DCC
neuropilins & plexins complex
TRR
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14
Q

Initial differentiation & axon extension of retina ganglion cells

A

RGC differentiate as wave, but neuroepitheliam next to wave is INHOSPITABLE because of chondrotin sulfate proteoglycan expression

–>RGC extend axon into optic fiber layer at inner surface of retina

–>Netrin/DCC & cell adhesion molecules attract axons to optic disc

–>run in optic stalk

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15
Q

how do RGCs known where to extend their axons?

A

integrins and cadherins!

and inhib actions of Slit-Robo in outer retina areas

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16
Q

Netrin

A

glial cells surrounding optic disc

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17
Q

DCC

A

R expressed by axons

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18
Q

RGC at brain after optic stalk

A

course towards ventral midline

  • ->optic chiasm
  • ->temporal retina (ipsilateral) & nasal retina (contralateral)
  • ->transition to targets
  • ->optic tracts
  • ->target (retinotopic maps)
19
Q

why can they project axons into optic chiasM?

A

decrease SHH at optic recess (which normally inhibits)

20
Q

temporal and nasal retina

A

ephrin B2/Eph B

NCAM/Sema3d

21
Q

Gap 43

A

allows to go from chiasm–>optic tract

22
Q

Slit/Robo

A

repellants to keep axons ont ract

23
Q

CSP6

A

keep axons from inappropriately crossing di/telencephalon

24
Q

what keeps axons in optic tract

A

cadherins and integrins

25
fibroblast growth factor
encourages axon extension | if low, encourages axon to stop and stay
26
Nasal RGC terminate in
posterior tectum
27
temporal RGCs terminate in
anterior tectum
28
ephrin A
highest in posterior tectum- repels temporal axons that express RGC meanwhile, eph A highest in temporal area
29
ephA
repels nasal, so since there is low epha in posterior axes-- nasal goes to posterior
30
dorsal RGC go to
medial region
31
ventral RGc go to
lateral region
32
ephrin B/eph B establish
dorsal/ventral axes
33
heparin sulfate proteoglycans
bind to regulate both location and signaling of slit/robo complexes
34
Slit
robo R | secreted by cells in midline to repel axons
35
Nextrin
binds with DCC | attracts axons early on
36
Robo/DCC
blocks netrin response
37
if robo/slit unopposed
no decussation
38
as axons reach midline,
expression of RObo 3 increased
39
ROBO 3
blocks ROBO 1 but does not interat with Netrin-->netrin/slit predominatea and cross midline
40
as cross, get increase sensitivty to
sema 3 repellant | further dissuades axons from turning back around
41
growth cone will turn towards a netrin gradient if
CAMP is high
42
inhibition of CAMp by pka
turns netrin from attraction to repulsion
43
horizontal gaze palsy with progressive scoliosis
mutation in robo3 abnormal morpholgy of abducents nucleus (hypoplasia) absence of normal decussation of corticospinal tract and/or ascending sensory information