von bartheld regeneration Flashcards
what comprises a bigger area/volume of the neuron: axon or cell body?
axon for sure
schematic
> =============================================================[cellbody] =============================================<
axonal injury in PNS:
- what o we call the degeneration of the distal stump of the lesioned axon?
- why do we call chromatolysis that name?
- when does axon growth occur?
- where does target re-innervation occur?
- Degeneration of the distal stump of a lesioned axon—aka wallerian degeneration
- Chromatolysis (Cell Body Response, cell body becomes much more pale compared to normal)
- Axon Growth (after injury)
- Target Re-innervation (in the PNS)
nissl stai
stain for nervous tissue sheaths
RER stains really well!
chromatolysis: when does it occur, what happens?
occurs when cell body responses to axotomy!!!!
Notice how you lost the nissl material and the cell body became paler. The gene expression profile gets changed.
These neurons sometimes struggle to stay alive.
time course or regeneration
you get chormatolysis early on
after two weeks, the lesioned cell starts forming a growth cone and attempts to bridge back
after 3 weeks, axon ends can meet if the conditions are right
after three months, the axons may fused together
^process depends on distance of lesion, how much nutrition/trophic factors available etc
wallerian degeneration:
-what’s the point of it?
In mouse mutant, a distal stump can stick around for 2-3 weeks but its regneration is slow.
Degeneration is now believed to be an active process that allows us to have a viable stump—schwann cells come in and then macrophages come too to degrade the myelin and cell remnants and then growth factors are prime for the growth cone to successfully come back .
explain wallerian degeneration from start to finsh
place special focus on bands of bunger
Active destructive Process (not due to loss of “nutrition” by anterograde transport)
- Breakdown of axonal Cytoskeleton
- Invasion of Macrophages (do not touch unlesioned axons tho)
- Removal of Myelin by Schwann cells
- Denervated Schwann cells secrete trophic factors, divide and form “bands of Bungner (make little path for hurt axons to go eventually go through)”
^Restricted to axotomized fibers – not intact ones
All these events promote the Regeneration Process (prepare pathway for axonal regeneration)
if cell body dies, can we regenerate successfully?
never!
sucessfull regneration depends on axon growht and fxnal connection w/ target too
what cells participate in myelinating axons during regneration process
only schwann
oligodendrocytes in the CNS suck at doing this
role of organization of nerve bundles in regneration
In PNS, we have bundles.
It’s important for stumps to be in the same fascicle as the target (so within the same perineurium bundle)—otherwise we can get spatially incorrect innervation
scenario: too much gap between proximal and distal stump
whaddowedoooooo !?!?!?1
If too much of a gap between distal and proximal stump, you can use a graft (like nervus suralis) which provides a good substrate
prognosis of crushed nerve
good!!!!
prognosis of severed nerves =====> may be good
successfull regneration of motor nerve
the ECM/ glial scaffold remains
also helps the proliferating scwhann cells regenerate the axons
this is good! it can even allow for growth cone to resupply the areas of distal nerve dendrites that were degraded away!
CNS axon degeration
why is it slow? three things
Removal of debris is slow
Growth cones hardly advance (leading to growth cone collapse)
Astrocytes form scar
also repellent cues are found int he oligodendrocytes but not really in scwhann cells
what is nogo? why is nogo important?
Nogo (membrane protein in oligodendrocytes – not Schwann cells)
Cells in KO nogo can lead to CNS regneration . we dunno how tho
CONCLUSION: nogo may decrease CNS regenereation
