Neuromuscular Blocking Drugs

Neuromuscular blocking drugs were first used by South American Indians on their arrows to paralyze their prey. During that time neuromuscular drugs were called curare. They were first written about in a letter by a chronicler, employed by the Court of King Ferdinand and Queen Isabella, in 1516. In the 18th century Edward Bancroft, a physician, brought samples of curare back from South America and Sir Benjamin Brodie showed how small animals could be left alive after being injected with curare and manually breathing for them. Further research continued and in 1846 Claude Bernard published details that when curare was injected into the nerve of a frog failed to abolish muscle contractions in response to either nerve stimulation or direct muscle stimulation, proof that curare acted at the nerve-muscle junction (Raghavendra, 2002, p. 363).
There are two groups of neuromuscular blockers, the depolarizers and the non- depolarizers. A few drugs that fall under the non-depolarizing agents are Tubocurarine, Gallamine, Pancuronium, Vecuronium, Atracurium, Mivacurium, and Rocuronium (Raghavendra, 2002, p. 364). A depolarizing drug is Succinylcholine. All of these are given as an injection as part of an anesthetic protocol (Saunders, 2013, p. 123c).
Both depolarizing and non-depolarizing agents bind to the motor end plate on the cell membrane of a dendrite that is on the next neuron and paralysis results from the blocking of a neurotransmitter transmission. Succinylcholine, the only depolarizing neuromuscular blocking drug, attaches to the chemical messenger receptor, also called a neurotransmitter receptor, at the motor end plate and changes the receptor to prevent the binding of acetylcholine, the neurotransmitter, to the receptor. When the depolarization occurs, when the voltage-sensitive sodium channels feel the depolarization of the membrane it opens and then closes and