The α9α10 acetylcholine receptor: A non-neuronal nicotinic receptor
- PMID: 36931539
- DOI: 10.1016/j.phrs.2023.106735
The α9α10 acetylcholine receptor: A non-neuronal nicotinic receptor
Abstract
Within the superfamily of pentameric ligand-gated ion channels, cholinergic nicotinic receptors (nAChRs) were classically identified to mediate synaptic transmission in the nervous system and the neuromuscular junction. The α9 and α10 nAChR subunits were the last ones to be identified. Surprisingly, they do not fall into the dichotomic neuronal/muscle classification of nAChRs. They assemble into heteropentamers with a well-established function as canonical ion channels in inner ear hair cells, where they mediate central nervous system control of auditory and vestibular sensory processing. The present review includes expression, pharmacological, structure-function, molecular evolution and pathophysiological studies, that define receptors composed from α9 and α10 subunits as distant and distinct members within the nAChR family. Thus, although α9 and α10 were initially included within the neuronal subdivision of nAChR subunits, they form a distinct clade within the phylogeny of nAChRs. Following the classification of nAChR subunits based on their main synaptic site of action, α9 and α10 should receive a name in their own right.
Keywords: Cochlea; Hair cells; Hearing; Ligand-gated channels; Nicotinic receptors.
Copyright © 2023 The Authors. Published by Elsevier Ltd.. All rights reserved.
Conflict of interest statement
Declarations of interest none.
Similar articles
-
Presence of multiple binding sites on α9α10 nAChR receptors alludes to stoichiometric-dependent action of the α-conotoxin, Vc1.1.Biochem Pharmacol. 2014 May 1;89(1):131-40. doi: 10.1016/j.bcp.2014.02.002. Epub 2014 Feb 15. Biochem Pharmacol. 2014. PMID: 24548457 Free PMC article.
-
Key role of the TM2-TM3 loop in calcium potentiation of the α9α10 nicotinic acetylcholine receptor.Cell Mol Life Sci. 2024 Aug 9;81(1):337. doi: 10.1007/s00018-024-05381-2. Cell Mol Life Sci. 2024. PMID: 39120784 Free PMC article.
-
A novel alpha-conotoxin, PeIA, cloned from Conus pergrandis, discriminates between rat alpha9alpha10 and alpha7 nicotinic cholinergic receptors.J Biol Chem. 2005 Aug 26;280(34):30107-12. doi: 10.1074/jbc.M504102200. Epub 2005 Jun 27. J Biol Chem. 2005. PMID: 15983035
-
The Hair Cell α9α10 Nicotinic Acetylcholine Receptor: Odd Cousin in an Old Family.Front Cell Neurosci. 2021 Nov 15;15:785265. doi: 10.3389/fncel.2021.785265. eCollection 2021. Front Cell Neurosci. 2021. PMID: 34867208 Free PMC article. Review.
-
Nicotinic acetylcholine receptors: from structure to brain function.Rev Physiol Biochem Pharmacol. 2003;147:1-46. doi: 10.1007/s10254-003-0005-1. Epub 2003 Mar 20. Rev Physiol Biochem Pharmacol. 2003. PMID: 12783266 Review.
Cited by
-
Inhibition of nicotinic acetylcholine receptors by oligoarginine peptides and polyamine-related compounds.Front Pharmacol. 2023 Dec 15;14:1327603. doi: 10.3389/fphar.2023.1327603. eCollection 2023. Front Pharmacol. 2023. PMID: 38169863 Free PMC article.
-
The Role of Alpha-7 Nicotinic Acetylcholine Receptors in Pain: Potential Therapeutic Implications.Curr Neuropharmacol. 2025;23(2):129-144. doi: 10.2174/1570159X22666240528161117. Curr Neuropharmacol. 2025. PMID: 38808717 Free PMC article. Review.
-
The Medial Olivocochlear Efferent Pathway Potentiates Cochlear Amplification in Response to Hearing Loss.J Neurosci. 2025 Apr 9;45(15):e2103242025. doi: 10.1523/JNEUROSCI.2103-24.2025. J Neurosci. 2025. PMID: 39984203
-
αO-Conotoxin GeXIVA[1,2] Reduced Neuropathic Pain and Changed Gene Expression in Chronic Oxaliplatin-Induced Neuropathy Mice Model.Mar Drugs. 2024 Jan 19;22(1):49. doi: 10.3390/md22010049. Mar Drugs. 2024. PMID: 38276651 Free PMC article.
-
Molecular determinants of the selectivity and potency of α-conotoxin Vc1.1 for human nicotinic acetylcholine receptors.J Biol Chem. 2025 Jan;301(1):108017. doi: 10.1016/j.jbc.2024.108017. Epub 2024 Nov 26. J Biol Chem. 2025. PMID: 39608712 Free PMC article.
Publication types
MeSH terms
Substances
Grants and funding
LinkOut - more resources
Full Text Sources