Wiring a Nervous System Flashcards
guidepost cels
direct outgrowing axons and change their direction
==>alter intracellular signaling with growth cones
pioneer neurons
first to grow in uncharted territory
growth cones are active filopodia
follower neurons
much simpler growth cones (fewer filopodia)–>latch to pioneers trail and form fasicles
some pioneer neurons
are transitory–they die and are replaced by permanent neurons
path finding neurons
developming neurons that respond to growth cones (lamellipodia and filopodia)
when they reach target they differentiate into pre syn terminals
trophic molecules
support growth and survival
tropic molecules
guide
extracellular matrix proteins
laminin, collagen, fibronectin
function of emp
interact with integrins on axon
- -regulate extend of adhesion of growth cones
- -allow to extend and pull axons along with them
cell adhesion molecules are used for
pioneer and follower neurons
what are cell adhesion molecules
CAM
Ca-indep
–act as both ligand and R
-hemophilic and heterophilic interactions
promote adherence amongst axon processes
chemoattractants/chemorepellants
slit ephrin netrin semaphorin neurotrophin
receptors
roundabout Eph DCC neuropilins & plexins complex TRR
Initial differentiation & axon extension of retina ganglion cells
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
how do RGCs known where to extend their axons?
integrins and cadherins!
and inhib actions of Slit-Robo in outer retina areas
Netrin
glial cells surrounding optic disc
DCC
R expressed by axons
RGC at brain after optic stalk
course towards ventral midline
- ->optic chiasm
- ->temporal retina (ipsilateral) & nasal retina (contralateral)
- ->transition to targets
- ->optic tracts
- ->target (retinotopic maps)
why can they project axons into optic chiasM?
decrease SHH at optic recess (which normally inhibits)
temporal and nasal retina
ephrin B2/Eph B
NCAM/Sema3d
Gap 43
allows to go from chiasm–>optic tract
Slit/Robo
repellants to keep axons ont ract
CSP6
keep axons from inappropriately crossing di/telencephalon
what keeps axons in optic tract
cadherins and integrins
fibroblast growth factor
encourages axon extension
if low, encourages axon to stop and stay
Nasal RGC terminate in
posterior tectum
temporal RGCs terminate in
anterior tectum
ephrin A
highest in posterior tectum- repels temporal axons that express RGC
meanwhile, eph A highest in temporal area
ephA
repels nasal, so since there is low epha in posterior axes– nasal goes to posterior
dorsal RGC go to
medial region
ventral RGc go to
lateral region
ephrin B/eph B establish
dorsal/ventral axes
heparin sulfate proteoglycans
bind to regulate both location and signaling of slit/robo complexes
Slit
robo R
secreted by cells in midline to repel axons
Nextrin
binds with DCC
attracts axons early on
Robo/DCC
blocks netrin response
if robo/slit unopposed
no decussation
as axons reach midline,
expression of RObo 3 increased
ROBO 3
blocks ROBO 1 but does not interat with Netrin–>netrin/slit predominatea and cross midline
as cross, get increase sensitivty to
sema 3 repellant
further dissuades axons from turning back around
growth cone will turn towards a netrin gradient if
CAMP is high
inhibition of CAMp by pka
turns netrin from attraction to repulsion
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
