Nicotinic acetylcholine receptor

Acetylcholine
Nicotine

Nicotinic acetylcholine receptors, or nAChRs, are receptor polypeptides that respond to the neurotransmitter acetylcholine. Nicotinic receptors also respond to drugs such as the agonist nicotine. They are found in the central and peripheral nervous system, muscle, and many other tissues of many organisms. At the neuromuscular junction they are the primary receptor in muscle for motor nerve-muscle communication that controls muscle contraction. In the peripheral nervous system: (1) they transmit outgoing signals from the presynaptic to the postsynaptic cells within the sympathetic and parasympathetic nervous system, and (2) they are the receptors found on skeletal muscle that receive acetylcholine released to signal for muscular contraction. In the immune system, nAChRs regulate inflammatory processes and signal through distinct intracellular pathways.[1] In insects, the cholinergic system is limited to the central nervous system.[2]

The nicotinic receptors are considered cholinergic receptors, since they respond to acetylcholine. Nicotinic receptors get their name from nicotine which does not stimulate the muscarinic acetylcholine receptors but selectively binds to the nicotinic receptors instead.[3][4][5] The muscarinic acetylcholine receptor likewise gets its name from a chemical that selectively attaches to that receptor—muscarine.[6] Acetylcholine itself binds to both muscarinic and nicotinic acetylcholine receptors.[7]

As ionotropic receptors, nAChRs are directly linked to ion channels. Some evidence suggests that these receptors can also use second messengers (as metabotropic receptors do) in some cases.[8] Nicotinic acetylcholine receptors are the best-studied of the ionotropic receptors.[3]

Since nicotinic receptors help transmit outgoing signals for the sympathetic and parasympathetic systems, nicotinic receptor antagonists such as hexamethonium interfere with the transmission of these signals. Thus, for example, nicotinic receptor antagonists interfere with the baroreflex[9] that normally corrects changes in blood pressure by sympathetic and parasympathetic stimulation of the heart.

  1. ^ Lu B, Kwan K, Levine YA, Olofsson PS, Yang H, Li J, et al. (August 2014). "α7 nicotinic acetylcholine receptor signaling inhibits inflammasome activation by preventing mitochondrial DNA release". Molecular Medicine. 20 (1): 350–8. doi:10.2119/molmed.2013.00117. PMC 4153835. PMID 24849809.
  2. ^ Yamamoto I (1999). "Nicotine to Nicotinoids: 1962 to 1997". Nicotinoid Insecticides and the Nicotinic Acetylcholine Receptor. pp. 3–27. doi:10.1007/978-4-431-67933-2_1. ISBN 978-4-431-68011-6.
  3. ^ a b Purves D, Augustine GJ, Fitzpatrick D, Hall WC, LaMantia AS, McNamara JO, White LE (2008). Neuroscience (4th ed.). Sinauer Associates. pp. 122–6. ISBN 978-0-87893-697-7.
  4. ^ Siegel GJ, Agranoff BW, Fisher SK, Albers RW, Uhler MD (1999). "GABA Receptor Physiology and Pharmacology". Basic Neurochemistry: Molecular, Cellular and Medical Aspects (6th ed.). American Society for Neurochemistry. Retrieved 2008-10-01. {{cite book}}: |website= ignored (help)
  5. ^ Itier V, Bertrand D (August 2001). "Neuronal nicotinic receptors: from protein structure to function". FEBS Letters. 504 (3): 118–25. Bibcode:2001FEBSL.504..118I. doi:10.1016/s0014-5793(01)02702-8. PMID 11532443.
  6. ^ Ishii M, Kurachi Y (1 October 2006). "Muscarinic acetylcholine receptors". Current Pharmaceutical Design. 12 (28): 3573–81. doi:10.2174/138161206778522056. PMID 17073660.
  7. ^ Lott EL, Jones EB (2020). "Cholinergic Toxicity". StatPearls. StatPearls Publishing. PMID 30969605.
  8. ^ Kabbani N, Nordman JC, Corgiat BA, Veltri DP, Shehu A, Seymour VA, Adams DJ (December 2013). "Are nicotinic acetylcholine receptors coupled to G proteins?". BioEssays. 35 (12): 1025–34. doi:10.1002/bies.201300082. PMID 24185813. S2CID 9441100.
  9. ^ Henderson CG, Ungar A (April 1978). "Effect of cholinergic antagonists on sympathetic ganglionic transmission of vasomotor reflexes from the carotid baroreceptors and chemoreceptors of the dog". The Journal of Physiology. 277 (1): 379–385. doi:10.1113/jphysiol.1978.sp012278. PMC 1282395. PMID 206690.