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I first thought that this is because of prolonged depolarisations. However, I am not sure anymore, because after reading PubChem, the only possible pathways are are Choline agonist. So I would say that succinylcholine cause myorelaxation by some cholino-receptor agonists. I do not think it is about depolarisation and how long it is.

How can succinylcholine cause myorelaxation?

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Succinycholine, as its name might suggest, is a cholinergic agonist indeed. It acts on the neural plate of skeletal muscles, where it activates the muscle cholinergic receptors.

Phase 1 block due to succinylcholine thus occurs by activating so many receptors at once, that the whole muscle gets desensitized and therefore paralyzed. A corollary of that is that muscle will twitch during activation, thus accounting for the reason why people twitch shortly before becoming paralyzed after a succinycholine iv injection. This phase 1 block will resolve in 2-5 minutes.

Now an interesting phenomenon is that if you go on stimulating the muscle with more cholinergic agonists (for example, a second iv dose of succinylcholine), you may end up provoking endocytosis and degradation of the cholinergic receptors. This is called phase 2 block, and in contrast to phase 1, it will take at least several hours to resolve. This is why we never use a second dose in the clinics, except in very special cases. You can also read about it all on wikipedia

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  • $\begingroup$ What is the event called that causes such a phenomena as phase 1 block and phase 2 block? Do other adrenoergic drugs and Cardiac drugs have such characteristics? How such an event documented for instance in PubChem, for instance in the link in the body of my question? I want to be aware of such events for each drug. $\endgroup$ Commented Jan 21, 2015 at 10:20
  • $\begingroup$ So the short answer to my question is that the succinylcholine cause myorelaxation because of cholino-receptor antagonism with big dose or second dose; stimulated by endocytes and degradation of the cholinergic receptors. $\endgroup$ Commented Jan 21, 2015 at 10:27
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    $\begingroup$ NOT THAT KIND OF CHOLINERGIC RECEPTOR!!! think autonomic nervous system, not autonomic nervous system... he is talking about nicotinic cholinergic receptor on the SKELETAL MUSCLE, not the muscarinic cholinergic receptors on cardiac conducting cells and muscle... this is a drug to temporarily paralyze the skeletal muscle for the sake of the surgeon doing the operation.. this is an anesthesia drug, not a cardiology drug... $\endgroup$ Commented Jan 22, 2015 at 0:25
  • $\begingroup$ secondly, this phase 1 vs phase 2 is to distinguish it from the curare-derived neuromuscular blockers which ONLY act as antagonists on the nicotinic cholinergic receptor (aka exhibit phase 2 type effects)... the phase-1/phase-2 type drugs are called depolarizing neuromuscular blockers... the curare derrived ones are nondepolarizing... here is an article listing more depolarizing types with this phase-1/phase2 type effects: en.wikipedia.org/wiki/… another example of a drug is Decamethonium $\endgroup$ Commented Jan 22, 2015 at 0:30
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    $\begingroup$ oops, for "typical psychotics" it's supposed to say "typical ANTIpsychotics"... $\endgroup$ Commented Jan 22, 2015 at 1:00

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