Editing Muscle relaxant (section)

==Neuromuscular blockers==
[[File:Synapse diag4.png|thumb|200px|Detailed view of a neuromuscular junction: {{olist
 |[[Presynaptic]] terminal
 |[[Sarcolemma]]
 |[[Synaptic vesicle]]
 |[[Nicotinic acetylcholine receptor]]
 |[[Mitochondrion]]
}}]]
{{main|Neuromuscular-blocking drug}}

Muscle relaxation and paralysis can theoretically occur by interrupting function at several sites, including the [[central nervous system]], [[myelin]]ated somatic nerves, unmyelinated motor nerve terminals, [[nicotinic acetylcholine receptor]]s, the motor end plate, and the muscle membrane or contractile apparatus. Most neuromuscular blockers function by blocking transmission at the end plate of the [[neuromuscular junction]]. Normally, a nerve impulse arrives at the motor nerve terminal, initiating an influx of [[calcium]] ions, which causes the [[exocytosis]] of [[vesicle (biology)|synaptic vesicles]] containing [[acetylcholine]]. Acetylcholine then diffuses across the synaptic cleft. It may be hydrolysed by [[acetylcholine esterase]] (AchE) or bind to the nicotinic receptors located on the motor end plate. The binding of two acetylcholine molecules results in a [[Protein conformation|conformational change]] in the receptor that opens the sodium-potassium channel of the nicotinic receptor. This allows {{chem2|Na+}} and {{chem2|Ca(2+)}} ions to enter the cell and {{chem2|K+}} ions to leave the cell, causing a depolarization of the end plate, resulting in muscle contraction.<ref>{{cite book |first1=C.R. |last1=Craig |first2=R.E. |last2=Stitzel |title=Modern Pharmacology with clinical applications |url=https://archive.org/details/modernpharmacolo00crcr |url-access=limited |publisher=Lippincott Williams & Wilkins |year=2003 |isbn=0-7817-3762-1 |page=[https://archive.org/details/modernpharmacolo00crcr/page/n344 339] }}
</ref> Following depolarization, the acetylcholine molecules are then removed from the end plate region and enzymatically hydrolysed by acetylcholinesterase.<ref name="MillerRD"/>

Normal [[end plate]] function can be blocked by two mechanisms. Nondepolarizing agents, such as [[tubocurarine]], block the [[agonist]], acetylcholine, from binding to nicotinic receptors and activating them, thereby preventing depolarization. Alternatively, depolarizing agents, such as [[succinylcholine]], are nicotinic receptor [[agonist]]s which mimic Ach, block muscle contraction by depolarizing to such an extent that it [[Nicotinic acetylcholine receptor#Receptor regulatation|desensitizes]] the receptor and it can no longer initiate an [[action potential]] and cause muscle contraction.<ref name="MillerRD"/> Both of these classes of neuromuscular blocking drugs are structurally similar to acetylcholine, the endogenous ligand, in many cases containing two acetylcholine molecules linked end-to-end by a rigid carbon ring system, as in [[pancuronium]] (a nondepolarizing agent).<ref name="MillerRD"/>

[[File:Pancuronium acetylcholine-highlighted.png|center|thumb|300px|Chemical diagram of [[pancuronium]], with red lines indicating the two acetylcholine "molecules" in the structure]]