How is mechanism of action of depolarizing agents (Succinylcholine)?

Attaches to the nicotinic receptor and acts like acetylcholine to depolarize the junction Unlike acetylcholine, which is instantly destroyed by acetylcholinesterase, the depolarizing agent persists at high concentrations in the synaptic cleft, remaining attached to the receptor for a relatively longer time and providing a constant stimulation of the receptor. The depolarizing agent first causes the opening of the sodium channel associated with the nicotinic receptors, which results in depolarization of the receptor (Phase I) This leads to a transient twitching of the muscle (fasciculations). Continued binding of the depolarizing agent renders the receptor incapable of transmitting further impulses With time, continuous depolarization gives way to gradual repolarization as the sodium channel closes or is blocked. This causes a resistance to depolarization (Phase II) and a flaccid paralysis. In flaccid paralysis, muscles lose their tone and reflexes, leading to a lack of voluntary movement and a soft or flabby appearance (molle) in the affected limbs