Neurobiology of nicotine dependence
- 18 July 2008
- journal article
- review article
- Published by The Royal Society in Philosophical Transactions Of The Royal Society B-Biological Sciences
- Vol. 363 (1507), 3159-3168
- https://doi.org/10.1098/rstb.2008.0095
Abstract
Nicotine is a psychoactive ingredient in tobacco that significantly contributes to the harmful tobacco smoking habit. Nicotine dependence is more prevalent than dependence on any other substance. Preclinical research in animal models of the various aspects of nicotine dependence suggests a critical role of glutamate, gamma-aminobutyric acid (GABA), cholinergic and dopamine neurotransmitter interactions in the ventral tegmental area and possibly other brain sites, such as the central nucleus of the amygdala and the prefrontal cortex, in the effects of nicotine. Specifically, decreasing glutamate transmission or increasing GABA transmission with pharmacological manipulations decreased the rewarding effects of nicotine and cue-induced reinstatement of nicotine seeking. Furthermore, early nicotine withdrawal is characterized by decreased function of presynaptic inhibitory metabotropic glutamate 2/3 receptors and increased expression of postsynaptic glutamate receptor subunits in limbic and frontal brain sites, while protracted abstinence may be associated with increased glutamate response to stimuli associated with nicotine administration. Finally, adaptations in nicotinic acetylcholine receptor function are also involved in nicotine dependence. These neuroadaptations probably develop to counteract the decreased glutamate and cholinergic transmission that is hypothesized to characterize early nicotine withdrawal. In conclusion, glutamate, GABA and cholinergic transmission in limbic and frontal brain sites are critically involved in nicotine dependence.Keywords
This publication has 79 references indexed in Scilit:
- Positive Modulation of GABAB Receptors Decreased Nicotine Self-Administration and Counteracted Nicotine-Induced Enhancement of Brain Reward Function in RatsJournal of Pharmacology and Experimental Therapeutics, 2008
- NMDA Receptors Regulate Nicotine-Enhanced Brain Reward Function and Intravenous Nicotine Self-Administration: Role of the Ventral Tegmental Area and Central Nucleus of the AmygdalaNeuropsychopharmacology, 2008
- Spontaneous Nicotine Withdrawal Potentiates the Effects of Stress in RatsNeuropsychopharmacology, 2007
- Syntheses and optimization of new GS39783 analogues as positive allosteric modulators of GABAB receptorsBioorganic & Medicinal Chemistry Letters, 2007
- Long-term effects of chronic nicotine exposure on brain nicotinic receptorsProceedings of the National Academy of Sciences of the United States of America, 2007
- Cystine/Glutamate Exchange Regulates Metabotropic Glutamate Receptor Presynaptic Inhibition of Excitatory Transmission and Vulnerability to Cocaine SeekingJournal of Neuroscience, 2005
- The GABAB Receptor-Positive Modulator GS39783 and the GABAB Receptor Agonist Baclofen Attenuate the Reward-Facilitating Effects of Cocaine: Intracranial Self-Stimulation Studies in the RatNeuropsychopharmacology, 2005
- A POTENTIAL ROLE FOR GABAB AGONISTS IN THE TREATMENT OF PSYCHOSTIMULANT ADDICTIONAlcohol and Alcoholism, 2002
- Differential effects of acute and chronic nicotine on dopamine output in the core and shell of the rat nucleus accumbensJournal of Neural Transmission, 1997
- Molecular and Cellular Aspects of Nicotine AbuseNeuron, 1996