Nicotinic acetylcholine receptor is an ion gated channel and I would like to know whether the allosteric modulation of this receptor will affect the GIT motility.

As GIT is innervated by sympathetic and parasympathetic innervation, will modulation of the nicotinic receptor increase the release of Ach, which then enhance the GIT motility?

If acetylcholinesterase inhibitor is given to gut tissue, it inhibits Ach breakdown and enhance the GIT contractility. So, I am interested to know whether allosteric modulation of the nicotinic receptor will influence GIT motility as well.

Hope to get fruitful insight from you! Thanks!