Journal
COLD SPRING HARBOR PERSPECTIVES IN MEDICINE
Volume 3, Issue 6, Pages -Publisher
COLD SPRING HARBOR LAB PRESS, PUBLICATIONS DEPT
DOI: 10.1101/cshperspect.a012146
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Funding
- NIH [1R01DA11946, R01DA232090, 2U19DA026838]
- Tobacco-Related Disease Research Program of the State of California [19FT-0045]
- Intracellular Therapeutics, Inc.
- Bristol-Myers Squibb Co.
- F. Hoffman-La Roche
- Pfizer
- Astra-Zeneca
- Abbott GmbH and Company
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Nicotine plays an important role in the initiation and maintenance of tobacco smoking. Importantly, chronic nicotine exposure alters the function of brain reward systems, resulting in the development of a nicotine-dependent state. This nicotine-dependent state is associated with aversive affective and somatic signs upon abstinence from smoking, often leading to relapse in abstinent smokers. This article reviews the role of the major excitatory and inhibitory neurotransmitters glutamate and gamma-aminobutyric acid (GABA), respectively, in both the reinforcing effects of nicotine and development of nicotine dependence. Evidence suggests that blockade of glutamatergic neurotransmission attenuates both nicotine intake and nicotine seeking. In contrast, both nicotine intake and nicotine seeking are attenuated when GABA neurotransmission is facilitated. In conclusion, medications that either attenuate/negatively modulate glutamatergic neurotransmission or facilitate/positively modulate GABA neurotransmission may be useful for promoting smoking cessation in humans.
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