<P> Depolarizing blocking agents work by depolarizing the plasma membrane of the muscle fiber, similar to acetylcholine . However, these agents are more resistant to degradation by acetylcholinesterase, the enzyme responsible for degrading acetylcholine, and can thus more persistently depolarize the muscle fibers . This differs from acetylcholine, which is rapidly degraded and only transiently depolarizes the muscle . </P> <P> There are two phases to the depolarizing block . During phase I (depolarizing phase), they cause muscular fasciculations (muscle twitches) while they are depolarizing the muscle fibers . Eventually, after sufficient depolarization has occurred, phase II (desensitizing phase) sets in and the muscle is no longer responsive to acetylcholine released by the motoneurons . At this point, full neuromuscular block has been achieved . </P> <P> The prototypical depolarizing blocking drug is succinylcholine (suxamethonium). It is the only such drug used clinically . It has a rapid onset (30 seconds) but very short duration of action (5--10 minutes) because of hydrolysis by various cholinesterases (such as butyrylcholinesterase in the blood). Succinylcholine was originally known as diacetylcholine because structurally it is composed of two acetylcholine molecules joined with a methyl group . Decamethonium is sometimes, but rarely, used in clinical practice . </P> <P> The main difference is in the reversal of these two types of neuromuscular - blocking drugs . </P>

The only depolarizing muscle relaxant in clinical use is