Nicotinic Acetylcholine receptors (nAchRs) belong to ligand-gated ion channels and are located within CNS and PNS and neuro-muscular junctions. Molecules that mimic the action of acetylcholine, bind to nAchRs and open the ion channels and allow an influx of sodium, potassium or calcium ions. The nAchR agonists include nicotine, acetylcholine, choline, cytisine, and epibatidine. Acetylcholine mainly acts through two different classes of receptors. These are nicotinic receptors (receptors in the skeletal muscle neuromuscular junctions and other ganglia and central nervous system) and muscarinic receptors (distributed in central and peripheral nervous system) (Role & Berg, 1996). Due to their strong affinity towards nicotine, acetylcholine receptors are commonly known as nicotinic acetylcholine receptors. In the peripheral nervous system, acetylcholine stimulates muscle contraction through its interaction with nAchRs in the skeletal muscle fibres.

Sodium ion channels are opened, and sodium influx occurs to initiate muscle contraction. It is to be noted that epibatidine has been found to be a potent agonist of nAchRs, though its application imparts profound peripheral effects as it also affects the nAchRs present in the muscular junctions. Therefore to come across its clinical limitations, nerve specific analogues are getting more familiar. ABT-594, an analogue of epibatidine, is currently in a clinical trial. In the treatment of dementia in Alzheimer’s disease, tobacco dependence, glaucoma, this group of drugs are mainly used. In contrast to this, drugs that selectively block the nicotinic receptors are known as ganglionic blocking agents or nicotinic antagonists.