Review Article
The Role of the Habenula in Nicotine Addiction
Philip R Baldwin1, Raul Alanis2 and Ramiro Salas2* | |
1Department of Neuroscience, Baylor College of Medicine, One Baylor Plaza, Houston TX 77030, USA | |
2Department of Psychiatry, Baylor College of Medicine, One Baylor Plaza, Houston TX 77030, USA | |
Corresponding Author : | Dr. Ramiro Salas Department of Psychiatry Baylor College of Medicine, One Baylor Plaza Houston TX 77030, USA Tel: 713-798-3846 Fax: 713-798-4488 E-mail: rsalas@bcm.edu |
Received August 02, 2011; Accepted October 17, 2011; Published October 22, 2011 | |
Citation: Baldwin PR, Alanis R, Salas R (2011) The Role of the Habenula in Nicotine Addiction. J Addict Res Ther S1:002.doi:10.4172/2155-6105.S1-002 | |
Copyright: © 2011 Baldwin PR, 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. | |
Related article at![]() ![]() |
Abstract
To thrive in any given environment, mobile creatures must be able to learn from the outcomes of both successful and disappointing events. To learn from success, the brain relies on signals originating in the ventral tegmental area and substantia nigra that result in increased release of dopamine in the striatum. Recently, it was shown that to learn from disappointment the brain relies on signals originating in the lateral habenula, which indirectly inhibit dopaminergic activity. The habenula is a small brain region that has been shown in mice to be critical for the appearance of nicotine withdrawal symptoms. The nicotinic acetylcholine receptor subunits expressed in the medial habenula are necessary to observe withdrawal symptoms in mice, and blocking nicotinic activity in the medial habenula only is sufficient to precipitate withdrawal in dependent mice. In addition, recent genome wide association studies have shown that in humans, genetic variants in the same nicotinic receptor subunits are at least partially responsible for the genetic predisposition to become a smoker. The habenula is linked not only to nicotine, but also to the effects of several other drugs. We postulate that the continuous use of drugs of abuse results in habenular hyperactivity as a compensatory mechanism for artificially elevated dopamine release. Drug withdrawal would then result in non-compensated habenular hyperactivity, and could be thought of as a state of continuous disappointment (or a negative emotional state), driving repeated drug use. We believe that drugs that alter habenular activity may be effective therapies against tobacco smoke and drug addiction in general.