The Unique α4(1)/(2)α4 Agonist Binding Site In (α4)3(β2)2 Subtype Nicotinic Acetylcholine Receptors Permits Differential Agonist Desensitization Pharmacology Versus The (α4)2(β2)3 Subtypes
Department
neurobiology
Document Type
Article
Abstract
Selected nicotinic agonists were used to activate and desensitize high-sensitivity (HS) (α4)2(β2)3) or low-sensitivity (LS) (α4)3(β2)2) isoforms of human α4β2-nicotinic acetylcholine receptors (nAChRs). Function was assessed using 86Rb1 efflux in a stably transfected SH-EP1-hα4β2 human epithelial cell line, and twoelectrode voltage-clamp electrophysiology in Xenopus laevis oocytes expressing concatenated pentameric HS or LS α4β2- nAChR constructs (HSP and LSP). Unlike previously studied agonists, desensitization by the highly selective agonists A-85380 [3-(2(S)-azetidinylmethoxy)pyridine] and sazetidine-A (Saz-A) preferentially reduced α4β2-nAChR HS-phase versus LS-phase responses. The concatenated-nAChR experiments confirmed that approximately 20% of LS-isoform acetylcholine-induced function occurs in an HS-like phase, which is abolished by Saz-A preincubation. Six mutant LSPs were generated, each targeting a conserved agonist binding residue within the LS-isoform-only α4(1)/(2)α4 interface agonist binding site. Every mutation reduced the percentage of LS-phase function, demonstrating that this site underpins LS-phase function. Oocyte-surface expression of the HSP and each of the LSP constructs was statistically indistinguishable, as measured using β2-subunit-specific [125I]μAb295 labeling. However, maximum function is approximately five times greater on a \"per-receptor\" basis for unmodified LSP versus HSP α4β2-nAChRs. Thus, recruitment of the α4(1)/(2)α4 site at higher agonist concentrations appears to augment otherwisesimilar function mediated by the pair of α4(1)/(2)β2 sites shared by both isoforms. These studies elucidate the receptor-level differences underlying the differential pharmacology of the two α4β2-nAChR isoforms, and demonstrate that HS versus LS α4β2-nAChR activity can be selectively manipulated using pharmacological approaches. Since α4β2 nAChRs are the predominant neuronal subtype, these discoveries likely have significant functional implications, and may provide important insights for drug discovery and development. Copyright © 2013 by The American Society for Pharmacology and Experimental Therapeutics.
Publication Date
1-1-2014
Publication Title
Journal of Pharmacology and Experimental Therapeutics
ISSN
00223565
Volume
348
Issue
1
First Page
46
Last Page
58
Digital Object Identifier (DOI)
10.1124/jpet.113.208389
Recommended Citation
Eaton, J. Brek; Lucero, Linda M.; Stratton, Harrison; Chang, Yongchang; Cooper, John F.; Lindstrom, Jon M.; Lukas, Ronald J.; and Whiteaker, Paul, "The Unique α4(1)/(2)α4 Agonist Binding Site In (α4)3(β2)2 Subtype Nicotinic Acetylcholine Receptors Permits Differential Agonist Desensitization Pharmacology Versus The (α4)2(β2)3 Subtypes" (2014). Translational Neuroscience. 285.
https://scholar.barrowneuro.org/neurobiology/285