So, as you may have guessed, Nicotinic M (Nm) Receptors are famous for their role in skeletal muscle movement! They are all over the motor end plates at the neuromuscular junctions of our skeletal muscles. So they are in charge of receiving the signals, via acetylcholine binding, to depolarize and contract! Nm Receptors have had a long history of being messed with in different ways, and it’s pretty awesome. But I digress…
These receptors are Ligand Gated Ion Channels. Remember those? If not, check out “Our Friends the Receptors” in the Basic Pharmacology section. The coolest thing about this type of receptor is that ligands (like Acetylcholine, or ACh) bind to them directly. That means there is no chain reaction that must occur (like the “second messengers” in GPCRs, think of that game called “Telephone“). The receptor simply changes its shape, and certain ions are allowed to flow in or out. Genius! But why is it so important to have this kind of receptor at the Neuromuscular Junction?
Ligand Gated Ion Channels are FAST. We need these because muscles need to quickly depolarize and repolarize to maintain a contraction or get ready for the next contraction.
Drugs that affect these receptors at the neuromuscular junctions either enhance the amount of ACh available (cholinesterase inhibitors), compete with ACh for binding (nondepolarizing neuromuscular blockers), or block ACh completely (depolarizing neuromuscular blockers).
Receptors never cease to amaze me. Humor me for a moment and watch your fingers type something. Then imagine how fast those ion channels are receiving signals and getting to work. Incredible! Now imagine what would happen if all of them were suddenly blocked. Besides how awful that would be, can you think of a good use for that trick?