alexa Nicotinic Acetylcholine Receptors in the Ventral Tegmental Area are Important Targets for Nicotine and Ethanol Co-dependence | OMICS International | Abstract
ISSN: 2167-0501

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Review Article

Nicotinic Acetylcholine Receptors in the Ventral Tegmental Area are Important Targets for Nicotine and Ethanol Co-dependence

Devin H. Taylor1,2, Scott C. Steffensen3 and Jie Wu1,2*
1Interdisciplinary Program in Neuroscience, Graduate College, Arizona State University, USA
2Division of Neurology, Barrow Neurological Institute, St. Joseph’s Hospital and Medical Center, USA
3Departments of Psychology, and Physiology & Developmental Biology, Brigham Young University, USA
Corresponding Author : Jive Wu, MD, Ph.D
Professor, Division of Neurology
Jie Barrow Neurological Institute
St. Joseph’s Hospital and Medical Center, USA
Tel: (602) 406-6376
E-mail: [email protected]
Received February 27, 2013; Accepted March 25, 2013; Published March 28, 2013
Citation: Taylor DH, Steffensen SC, Wu J (2013) Nicotinic Acetylcholine Receptors in the Ventral Tegmental Area are Important Targets for Nicotine and Ethanol Codependence. Biochem Pharmacol (Los Angel) S1:002. doi:10.4172/2167-0501.S1-002
Copyright: © 2013 Taylor DH, 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.

Abstract

Tobacco and alcohol are the most commonly abused drugs. The nicotine (NIC) in tobacco and the ethanol (EtOH) in alcoholic drinks are responsible for their dependence respectively. The magnitude of tobacco smoking is drastically higher among alcoholics, suggesting a NIC-EtOH co-dependence. However, the mechanisms of NIC-EtOH interaction are not fully known, and the clarification of this action is clinically relevant. The majority of the NIC-EtOH interaction utilizes the ventral tegmental area (VTA) through both dopamine (DA) and non-DA systems. EtOH has been shown to bind directly to some nicotinic acetylcholine receptors (nAChRs) as, of course, does NIC. The non-selective/noncompetitive
nAChR antagonist mecamylamine (MEC) has been shown to partially block the DA releasing action of EtOH in the nucleus accumbens (NAc), while both the α4β2 nAChR antagonist dihydro-β-erythroidine (DHβE) and the α7 nAChR antagonist methyllycaconitine (MLA) do not. However, the α6-containing nAChRs (α6*-nAChRs) are responsible for both NIC-induced effects on DA release in the NAc and EtOH-induced GABA release in the VTA, suggesting that the α6*-nAChRs likely play a significant role in NIC-EtOH interactions. In this review, we have summarized current studies that reveal how EtOH reward through VTA nAChRs and what nAChR subtypes play roles in mediation of EtOH’s effects
in mesolimbic circuits. The accumulating lines of evidence suggest that the nAChRs, especially α6*-nAChRs in the VTA are likely important targets for NIC-EtOH interactions and NIC-EtOH co-dependence.

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