During surgery it is often necessary to achieve dense-muscle relaxation to facilitate surgical technique or to ensure patient safety. To this end, the use of neuromuscular blocking agents have become an integral part of a balanced anesthetic technique. The two main classes of neuromuscular relaxing agents are the depolarizing muscle relaxants and the nondepolarizing muscle relaxants. Depolarizing agents mimic the action of acetylcholine at the neuromuscular junction (NMJ) and prevent the normal recovery of the muscle unit from its refractory state, rendering it unexcitable. Depolarizing relaxation is terminated when the agent diffuses from the neuromuscular junction to the plasma, where it is metabolized by plasma pseudocholinesterases. In contrast, nondepolarizing agents work as competitive antagonists of acetylcholine (ACH) at the NMJ. Their effects dissipate either when the drug diffuses away from its site of action or when there is an effective surge of ACH at the neuromuscular junction that competitively displaces the agent. The latter mechanism is the principle behind reversal of nondepolarizing neuromuscular blockade.

To briefly review, during normal transmission of an action potential, influx of calcium at the nerve terminal triggers the release of storage vesicles containing acetylcholine. The membrane packages diffuse across the synaptic cleft to bind with the ACH receptors at the motor endplate. This binding results in a conformational change in the ligand-activated receptor at the motor endplate that allows the influx of ions, producing a depolarization of the motor endplate. When the membrane depolarization reaches a threshold, an action potential is produced and the muscle fiber fires. Stimulation is terminated when ACH is degraded by acetylcholinesterase located at the neuromuscular junction.