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Does this impulse in skeletal muscle spread much in the same way it does in neurons, with an initial potential change that spreads to its immediate surroundings and is then re-amplified or is it the case that in muscle fibers, the initially produced end plate potential must be "enough" to depolarize the whole muscle fiber?

My issue is with this bit in a lecture about NMJs I took:

Because the ACh-gated ion channels are localized to the end plate membrane, the End Plate Potential (EPP) is generated at and confined to the end plate region only and, therefore, the amplitude of EPP declines progressively with increasing distance from the end plate region.

I only found this site which talked about something similar, and there it talked about it in the context of a muscle fiber that's been blocked by a non-depolarizing neuromuscular blocker, i.e., no contraction occurs, it's just a measurement of how the EPP changes by itself, so perhaps the lecture was talking about something similar?

So, to put it simply, do electrical signals in skeletal muscles get re-amplified as they travel along the fiber, like they do with neuronal action potentials, or is the initial membrane potential sufficient and it just "spreads around"?

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Skeletal muscle cells are excitable, like neurons. Enough summation of end-plate potentials causes the cell to reach threshold and fire an action potential (which then spreads throughout the cell membrane through positive feedback, just like a neuronal action potential).

There are some differences between skeletal muscle and typical neurons, like greater importance of chloride in setting resting potential in muscles, but otherwise their action potentials are driven by voltage-gated sodium channels, just like typical neurons.

You quote:

the amplitude of EPP declines progressively with increasing distance from the end plate region.

which is true as long as the threshold potential isn't reached, and would also be true for subthreshold receptor potentials or post-synaptic potentials in neurons.

In the reference you link to, I assume you are referring to the mention of curare. Curare blocks the nicotinic acetylcholine receptor, so it is interfering with the end-plate potentials themselves, rather than the intrinsic excitability of the muscle.


See:

Philip M Hopkins, Skeletal muscle physiology, Continuing Education in Anaesthesia Critical Care & Pain, Volume 6, Issue 1, February 2006, Pages 1–6, https://doi.org/10.1093/bjaceaccp/mki062

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