Question about nerve polarization

This forum made possible through the generous support of SDN members, donors, and sponsors. Thank you.

tripkramer

New Member
10+ Year Member
Joined
Feb 28, 2013
Messages
7
Reaction score
0
What happens if there is excess acetylcholine in the nerve junction, possibly by a lack of working acetylcholinesterase?

I've read differing statements:

1. Constant depolarization (unable to repolarize) -> tonus or tetany
2. Increase in frequency of depolarization and action potential

So I guess basically the question is if the nerve can repolarize after depolarizing that first time?

Thanks!
 
I dont think 1 is necessarily true. There would probably be a higher frequency of EPSPs / action potentials, but tetanus is usually created from intense shocks where it would stay really depolarized.
 
Yes, a problem with degrading acetylcholine, such as a problem with acetylcholinesterase, would increase activity.

In terms of tetanus, I guess it depends first on the refractory period. You definitely do get sustained muscle contraction if the stimulus is frequent enough, because the refractory period becomes much shorter than the time required to contract/relax. It might also depend on muscle type. I know cardiac muscle does not undergo tetanus at all, and I may have read smooth muscle only undergoes incomplete tetanus, with brief periods of relaxation in between contractions.
 
by nerve junction I'm just assuming you're referring to the "neuromuscular junction" and "motor end plate"? your question is about muscle stimulation by acetylcholine?

This essentially applies to voluntary skeletal muscle. In theory, if acetylcholinesterase is completely inhibited and Ach is allowed to persist unwanted at the motor end plate, it will continually stimulate nicotinic Ach receptors. This increases the frequency of action potential to a maximum, but this is limited by a refractory period as you know. This excessive stimulation of the muscle fiber leads to tonus/tetany of the muscle which eventually fatigues and becomes paralyze. This type of mechanism is the main function of some therapeutics as well as toxins, as is the case for many substances. Succinylcholine is used
clinically as a depolarizing paralytic to eliminate muscle tone in procedures like intubation or ETC. These drugs can be dangerous to person succceptible to something called Malignant Hyperthermia however. As far as toxins go, this is basically the MOA of nerve gases used during wartime. Look up the mechanism of organophosphate poisoning
 

Similar threads

Top