A Signal Peptide Missense Mutation Associated With Nicotine Dependence Alters α2*-Nicotinic Acetylcholine Receptor Function
Department
neurobiology
Document Type
Article
Abstract
A cytosine to thymidine (C → T) missense mutation in the signal peptide (SP) sequence (rs2472553) of the nicotinic acetylcholine receptor (nAChR) α2 subunit produces a threonine-to-isoleucine substitution (T22I) often associated with nicotine dependence (ND). We assessed effects on function of α2*-nAChR ('*'indicates presence of additional subunits) of this mutation, which could alter SP cleavage, RNA/protein secondary structure, and/or efficiency of transcription, translation, subunit assembly, receptor trafficking or cell surface expression. Two-electrode voltage clamp analyses indicate peak current responses to ACh or nicotine are decreased 2.8-5.8-fold for putative low sensitivity (LS; 10:1 ratio of α:β subunit cRNAs injected) α2β2- or α2β4-nAChR and increased for putative high sensitivity (HS; 1:10 α:β subunit ratio) α2β2- (5.7-15-fold) or α2β4- (1.9-2.2-fold) nAChR as a result of the mutation. Agonist potencies are decreased 1.6-4-fold for putative LS or HS α2(T22I)β2-nAChR or for either α2*-nAChR subtype formed in the presence of equal amounts of subunit cRNA, slightly decreased for LS α2(T22I)β4-nAChR, but increased 1.4-2.4-fold for HS α2(T22I)β4-nAChR relative to receptors containing wild-type α2 subunits. These effects suggest that the α2 subunit SP mutation generally favors formation of LS receptor isoforms. We hypothesize that lower sensitivity of human α2*-nAChR to nicotine could contribute to increased susceptibility to ND. To our knowledge this is the first report of a SP mutation having a functional effect in a member of cys-loop family of ligand-gated ion channels. © 2014 Elsevier Ltd. All rights reserved.
Publication Date
4-1-2014
Publication Title
Neuropharmacology
ISSN
00283908
Volume
79
First Page
715
Last Page
725
Digital Object Identifier (DOI)
10.1016/j.neuropharm.2014.01.021
Recommended Citation
Dash, Bhagirathi; Lukas, Ronald J.; and Li, Ming D., "A Signal Peptide Missense Mutation Associated With Nicotine Dependence Alters α2*-Nicotinic Acetylcholine Receptor Function" (2014). Translational Neuroscience. 182.
https://scholar.barrowneuro.org/neurobiology/182