It has been so long to understand this transparently, It helped a lot,thank you

thank you so much for these videos

Thank you so much! *lightbulb*

Is this the reason why you have the Phase II pattern in depol. mm blocker? In the beginning massive ACh release due to succinylcholine stim pre-syn receptors, then less is available hence lower amplitude of T2, then even less for T3, and finally least for T4? EDIT: Ah, wait, I think I know why: First it's like described in the video, massive succinylcholine-med. presynaptic receptor activation leading to massive ACh release => twitch, probably always same intensity (that's why the train of four ratio is 1 in phase I?); but after a time succinylcholine binds also to some of the postsynaptic receptors, activating it but essentially making them useless (bcs they don't have the time to reset); as more succinylcholine binds "irreversibly" (bcs it's not degraded by acetylcholinesterase in the synaptic cleft) to more postsynaptic receptors even more of these receptors become useless, and again, even more binds and even more become useless, until no more receptors work. This progressive decrease in working receptors explains the "fade" pattern of the "phase II-block", right? Anyone verify please? :D EDIT2: Is it maybe possible that the theory in the video is outdated? Bcs tmedweb.tulane.edu/pharmwiki/doku.php/depolarizing_nm_blocker writes: "[...] In the motor endplate it [succinylcholine] combines with nicotinic receptors to produce depolarization which can be observed as uncontrolled focal muscle contractions (fasciculations). Subsequent transmission across the NMJ is inhibited as long as succinylcholine remains at the nicotinic receptor sites. A depolarized post-junctional membrane (resulting in inactivation of Na channels) causes the postjunctional membrane to become unresponsive to ACh released by motor neurons. This is referred to as “Phase I block” & produces a characteristic reduction in contractile response (with no fade) during a train of four stimuli. In less than a minute after IV administration a flaccid paralysis develops due to the development of a desensitized state where the membrane becomes repolarized, but insensitive to ACh (due to receptor desensitization). This is referred to as “Phase II block” and responds to a train of four stimuli with a “fade” pattern similar to that produced by non-depolarizing neuromuscular blockers. [...]" Any info, anyone? :-/ Final EDIT: I managed to ask my professor today - the mechanism (at least current consensus) behind succinylcholine-ind. fascicul is indeed the one explained in the link I posted, i.e. it's due to activation of POSTSYNAPTIC receptors (NOT due to massive ACh release via activating presynaptic receptors as stated in the video). Hope this helps

thank u ..it was helpfull

Thank u

what does nn and nM stand for? Neural muscular and nerual neuronal?

I wanna know why succinylcholine does not block synapse instead of pre synapse?

Y are fking good =D

It doesnt help. Sorry. (twitching already 29 years, every min +/- 7 times) There are multiple possible causes, but it's not clear yet. 'it's "benign" so no hurry for medical word' The fact that you go mental because of the twitching is forgotten!! :O

Made no sense at all