Abstract
Studies with rodent models have shown that, in addition to the nicotinic cholinergic system, nicotine withdrawal involves adaptations of dopamine, serotonin, norepinephrine, glutamate, gamma-aminobutyric acid (GABA), endogenous opiate, neuropeptide FF, neuropeptide Y, and still other synaptic transmission systems. In some cases, these may contribute differentially to different nicotine withdrawal phenomena. For example, α4β2 nicotinic acetylcholine receptors may be critical for depression-like or anhedonic effects, while α3β4 receptors may be more involved with measures reflecting irritability, such as hyperalgesia and somatically expressed withdrawal behaviors. Thus, there is a link between the diversity of neurochemical adaptations and the diversity of nicotine withdrawal signs and symptoms.
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