von bartheld plasticity Flashcards
neurotrophic hypothesis
We generate more neurons than are actually needed.
As neurons go to target cells they compete for trophic factors on the target molecules, and only a few of the early neurons (50-60 percent will actually survive)
trophic factors get retrogradedly transported–they help for survival
expt:
maniupltion of targets effect on neuronal cell bodies
Exp: manipulate target size of chicken embryos. They will ablate limb bud. In the ventral horn of the spinal cord they saw less motor neurons for that limb, compared to the unaffected normal side.
Can also transplate limb bund, and notice that there were more motor neurons in the spinal cord.
profile vs 3d counting. whichon e is better?
3d
coz profile counting can overcount.
a proflile = the number of things seen in the slices of the cut
big error = too many profiles for the number of objects
three fxns of neurotrophins
Survival
Differentiation
Synaptic Plasticity
neurotrophins bind to two types of receptors. what are they?
Neurotrophins bind to two types of cell surface receptors: Trk[A-C] or p75…. The trks are tyrosine kinase
throw out some families of trophic factors
Neurotrophins (NGF-like Factors)
GDNF-like Trophic Factors
FGF- (fibroblast growth factors)
IGFs (insulin-like growth factors)
signaling endosome fxn
Cell membrane forms a little vesicle, which binds to a receptor which is a transmembrane protein (this one carries the neurotropin within the endosome). And then that pinches off becomes a signaling endosome, and then travels in retrograde direction toward the cell body along microtubules.
Microtubule can go in the retrograde or other direction (it’ll go retrograde toward the cell body tho). The neurotropin has various signaling abilities once it goes to the receptor.
HTT
There’s a protein called HTT, hutington associated protein which is reponsible for a ton of cargo including trophic factors.
In huntingtons disease the HTT is mutated. In huntigintons chorea you also have LESS neurotrophin factors in the straitum.
Huntington’s is also known to enhance transport of cargo through mol motor mech—hypothesis is that the striatum doesn’t get as much trophic factors as it needs.
BDNF fxn
BDNF induces dendritic growth
general signaling cascade of the trk and the p75
^the receptors for the neurotrophins
We have two different receptors: trk and p75
Bind the ligand in trk -> tyr kindase activated –> and then that can go to various, three diff ones, pathways. All end up activating gene transcription!
Binding to p75 when it has traf with it =====> apoptosis
(note: NT on p75 may cause neuronal growth, but only if it lacks the TRAF)
polyneural innervation ====> fate?
In development, we have initially polyneural innervation—innervation of the same cell/fiber by multiple neurons.
In the mature fibers, we have 1:1.
It’s thought that polyneural cells compete for each other. During period of competition, the one with weakest input will lose out.
how did we find transneuronal transport in experiments?
Inject isotope into retina, and then retina cells will take that up and then transport it anterogrande to the thalamus and then the thalamus neurons transport it to the cortex.
define: ocular dominance column
Ocular dominance columns are stripes of neurons in the visual cortex of certain mammals (including humans) that respond preferentially to input from one eye or the other
what did they see when they gave radioactive proline to an eye?
eye —> LGN –> visual cortex
What they saw is that half of the cortex labeled coz in layer four the are not yet segregated
About 50 percent is labeeld and 50 percent is not.
These are called ocular dominant columns
development of ocular dominance column
Two weeks after birth, there Is no segregation in layer four. There is almost complete overlap in how right and left eye terminate at this point.
At six weeks you start to see that there are areas of overlap.
At thirteen weeks they are almost completely segregated in visual cortex
