THE NEUROMASCULAR JUNCTION IMPULSE TRANSMITION

 

Introduction:  Skeletal muscle relaxation and paralysis can occur from interruption of function at several sites along the pathway from the central nervous system (CNS) to myelinated somatic nerves, unmyelinated motor nerve terminals, nicotinic acetylcholine receptors, the motor end plate, the muscle membrane, and the intracellular muscular contractile apparatus itself.  Blockade of end plate function can be accomplished by two basic mechanisms. Pharmacologic blockade of the physiologic agonist acetylcholine is characteristic of the antagonist neuromuscular blocking drugs (ie, nondepolarizing neuromuscular blocking drugs). These drugs prevent access of the transmitter to its receptor and thereby prevent depolarization. The prototype of this nondepolarizing subgroup is d-tubocurarine.   The second type of blockade can be produced by an excess of a depolarizing agonist, such as acetylcholine. This seemingly paradoxical effect of acetylcholine also occurs at the ganglionic nicotinic acetylcholine receptor. The prototypical depolarizing blocking drug is  succinylcholine.  A similar depolarizing block can be produced by acetylcholine itself when high local concentrations are achieved in the synaptic apparatus.

RELATED;

1.  THE MECHANISM OF IMPULSE PROPAGATION

2.  SYNAPSES

3.  THE NEUROTRANSMITTER SYSTEMS

4.  DIVISIONS OF THE NERVOUS SYSTEM