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nwinkelmann
This really helped me, at least the pictures did. Here's my interpretation of the pictures in not super scientific terms: capacitance is like the "capaciy" to keep ions close to the membrane. Myelin puts a barrier between the ions in the conductive environment (ECF or ICF) and the nerve membrane. The higher the capacitance, the closer the ions are to the membrane, so it's like the charge effect is "more potent" so harder to change the membrane potentia, whereas if the ions are farther from the membrane, the charge effect is "less potent" so easier to change the membrane potential and thus easier to depolarize. Thus, with myelin, there is decreased capacity of the ions to be close to the membrane, so in demyelinating conditions, the ions can be really close to the membrane, i.e. higher capacitance.
+30
imgdoc
Just to add to what nwinkelmann said and elaborate further on the link by mcl. In neuronal axons, capacitance keeps ions close to the membrane (anions and cations), so when axon depolarization does occur, a portion of the cations meant to depolarize the axon will actually be neutralized by the anions at the membrane. MYELINATED axons basically provide a barrier so that there are LESS anions lining the inner surface of the axon membrane, so LESS cations get neutralized by the negative anions, so MORE cations are AVAILABLE to depolarize the axon. Now, membrane resistance: myelin increases axonal resistance, this means it DECREASES the ability of cations that entered the axon from LEAKING back out into the ECF. MORE cations are available to depolarize the neuronal axon.
MYELINATED AXONS INCREASE RESISTANCE, and DECREASE CAPACITANCE.
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For the video provided, skip to 4:25 for the description on capicitance
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littletreetrunk
I think this makes total sense, but how does it not ALSO stop fast axonal transport?
+5
laminin
axonal transport is transport of organelles bidirectionally along the axon in the cytoplasm since myelin is on the outside of the axon demyelination doesn't affect this process.
source: https://en.wikipedia.org/wiki/Axonal_transport
"Axonal transport, also called axoplasmic transport or axoplasmic flow, is a cellular process responsible for movement of mitochondria, lipids, synaptic vesicles, proteins, and other cell parts to and from a neuron's cell body, through the cytoplasm of its axon."
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yotsubato
axonal transport is mediated by kinesin and dynein. Microtubule toxins like vincristine block these
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drdoom
@littletreetrunk "axonal transport" is movement of bulk goods via microtubules (which run from soma to terminus); ions, on the other hand, move in an "electrical wave" that we call an action potential! no axonal (microtubular) transport required! in other words, de-myelination will have no effect on the transport of bulk goods; but it will really mess up how fast "electrical waves" traverse the neuron!
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handsome
what's your reference to this DOC
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diabetes
i think it slows down ,no cessation .
+1
gdupgrant
Because fast axonal transport refers to the transport of vesicles containing neurotransmitters or some kind of cell product up and down microtubules in the axon. It isn't related to actual electrical signal transduction.
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kcyanide101
Basically a summary of it all is the myelin sheeth creates a insulation which reduces capicatnace and increases resistance..... This causes charges not to leak as they then accumulate in the nodes of ranvier. Essential transmission is faster because the only leaking occurs between the myelin sheath (where ion exchanges occur),
https://www.youtube.com/watch?v=_Lj_F9GADa4
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kcyanide101
so just imagine the ion flow charges are jumping from one node of ranvier to the next
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submitted by โmcl(671)
In case you wanna go super nerd and read about myelin, capacitance, and resistance, this guy does a good job.