Neurochemical Transmission: Sites of Drug Action

Neurotransmission, the conduction of electrical impulses between neurons, mediates via neurotransmitters.

Autonomic drugs modulate neurotransmission in the autonomic nervous system.

For example, α-methyltyrosine inhibits neurotransmitter biosynthesis, while vesamicol and reserpine prevent its storage in synaptic vesicles.

The arrival of electrical impulses at the presynaptic axonal terminals results in Ca²⁺ influx and release of neurotransmitters by exocytosis into the synaptic cleft. This process is inhibited by botulinum toxin and guanadrel. However, it is accelerated by latrotoxin and amphetamine.

Released neurotransmitters bind specific receptors on the postsynaptic neuron to produce desired responses.

These receptors can be activated using specific drugs such as nicotine or methacholine, which mimics the neurotransmitters.

The receptors can be blocked by antagonists such as tubocurarine or atropine.

Following transmission, the reuptake of neurotransmitters into the presynaptic neurons is inhibited by drugs such as hemicholinium and cocaine, thereby prolonging neurotransmitter action.