Muscarinic M1 Gq protein coupled – second messenger is IP3,    increase intracellular calcium

  • Increased cognitive function, eg. memory
  • Increased seizure activity

Muscarinic M2 Gi protein coupled – inhibit adenylyl cyclase, decrease cAMP

  • Miosis (contraction) of the pupillary sphincter muscle
  • Contraction of the ciliary muscle for far vision
  • Lacrimal gland secretion
  • Significant reduction in heart rate
  • Significant reduction in atrial contractility, and shortened action potential duration
  • Significant reduction in the conduction velocity of the AV node
  • Slight decrease in ventricular contractility
  • Increased motility and tone of the stomach
  • Relaxation of gastric sphincters
  • Stimulation of gastric secretion
  • Contraction of the gallbladder
  • Relaxation of the intestinal sphincters, and increased intestinal motility

 

Muscarinic M3 Gq protein coupled – second messenger is IP3,    increase intracellular calcium

  • Miosis (contraction) of the pupillary sphincter muscle
  • Contraction of the ciliary muscle for far vision
  • Lacrimal gland secretion
  • Salivation and dilation of the salivary ducts
  • Greatly increased nasal mucus secretion
  • Increased production of nitric oxide synthase by the vascular endothelium
  • Increased motility and tone of the stomach
  • Relaxation of gastric sphincters
  • Stimulation of gastric secretion
  • Contraction of the gallbladder
  • Relaxation of the intestinal sphincters, and increased intestinal motility
  • Bladder detrusor muscle contraction, and relaxation of the trigone sphincter
  • Erection
  • Generalised secretion of the sweat glands (not just sweaty palms, but all over)
  • Increased secretion of the pancreatic juice

 

Muscarinic M4 Gi protein coupled – inhibit adenylyl cyclase, decrease cAMP

  • Inhibition of neurotransmitter release in the CNS
  • Facilitates Dopamine release

Muscarinic M5 Gq protein coupled – second messenger is IP3,    increase intracellular calcium

  • Facilitates Dopamine release
M1, M3 and M 5 are Gq protein coupled: the second messenger is IP3, and the result is calcium release.
In general, the rule of thumb for these receptors is the excitation of excitable tissue, and the activation of various glandular and secretory function.

Most glandular cells, posed with a massive influx of diacylglycerol and IP3 will begin to secrete stuff. Similarly, smooth muscle will contract when there is a calcium influx.

M1 M3 and M5 receptor intracellular signalling pathway

 
M2 and M4 are Gi protein coupled: they deactivate adenylyl cyclase, and decrease the levels of cAMP.

Broadly speaking, these receptors are membrane stabilizers.

Excitable tissues hyperpolarize, inward rectifying potassium currents start flowing, voltage-gated calcium channels are inhibited.

M2 and M4 receptor intracellular signalling pathway

These are ligand-gated sodium channels (more accurately, cation channels)
nicotinic receptor intracellular signalling pathway

There are several varieties; structurally they are sufficiently different to bind different drugs.

The receptor species at the neuromuscular junction is distinct from the species you will find at the autonomic ganglia.

Yes, Nicotine is an agonist for both neuronal and neuromuscular subtypes of nicotinic acetylcholine receptors.

These receptors cause a RAPID increase in membrane permeability to sodium and calcium. The door is open for less than a millisecond.

During that time, some 50,000 sodium ions force their way into the cell, causing immediate depolarization of the membrane.

The channel is not particularly selective; while it is open, potassium is able to escape from the cell. This is the channel feature which causes suxamethonium-induced hyperkalemia.

The structure of these receptors is pentameric.

nicotinic receptor structure

All of them have  5 subunits.

For the neuromuscular junction receptors, the five subunits are beta, delta epsilon and two alpha-1

The two alpha-1 subunits act as the binding sites of acetylcholine as well as the whole lot of neuromuscular blocking agents.

For the autonomic ganglia receptors, the five subunits are three beta and two alpha-3

The two alpha-3 subunits also act as binding sites for acetylcholine, but they will not bind neuromuscular blocking agents.

References

For this sort of really basic stuff, no matter where you look you will find essentially the same information.


I used chapters from "Goodman & Gilman's The Pharmacological Basis of Therapeutics" 11th ed by Brunton et al, and "Basic & Clinical Pharmacology" 11th ed. By Katzung et al.

I also perused Peck and Hill "Pharmacology for Anaesthesia and Intensive care" as well as the notoriously error-prone "Handbook of Pharmacology and Physiology in Anaesthetic Practice" by Stoelting and Hillier. Neither covered this subject in a depth I found satisfying.

Goodman and Gilman's remains a canonical text.