Targeting the α 4 β 2- and α 7-Subtypes of Nicotinic Acetylcholine Receptors for Smoking Cessation Medication Development
Received Date: Jan 21, 2019 / Accepted Date: Apr 08, 2019 / Published Date: Apr 15, 2019
Nicotine exerts its reinforcing actions via activating the nicotinic acetylcholine receptors (nAChRs). Among an increasing number of nAChR subtypes, the α4β2 and α7 nAChRs are the two major ones, accounting for about 95% of the whole nAChR population in brain. Research findings from our own laboratory, together with other reports in the field, suggest critical and differential involvement of the α4β2 and α7 nAChRs in the process of nicotine dependence and tobacco addiction. Specifically, rat models of nicotine consumption and cue-induced relapse were used to examine the effects of selective antagonism of these two nAChR subtypes on the primary reinforcement of nicotine and the conditioned reinforcing actions of nicotine-associated environmental stimuli (cues). Results demonstrated that blockade of the α4β2 but not α7 subtype effectively reduced nicotine intake, whereas α7 but not α4β2 nAChR blockade reversed cue-triggered nicotine relapse behavior. These findings lend support for the continued effort to develop cholinergic agents aiming at the α4β2 nAChRs for reducing or stopping smoking. However, it is suggested that manipulation of α7 nAChR activity would be a promising target for preventing smoking relapse triggered by exposure to environmental cues.
Keywords: Conditioned stimuli (cues); Nicotinic acetylcholine receptors (nachrs); Reinforcing actions; Relapse; Self-administration
Citation: Nair LR, Liu X (2019) Targeting the α4β2- and α7-Subtypes of Nicotinic Acetylcholine Receptors for Smoking Cessation Medication Development. J Addict Res Ther 10:381. Doi: 10.4172/2155-6105.1000381
Copyright: © 2019 Nair LR, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution and reproduction in any medium, provided the original author and source are credited.
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