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Abstract
A major hurdle in defining the molecular biology of nicotine addiction has been characterizing
the different nicotinic acetylcholine receptor (nAChR) subtypes in the brain and how
nicotine alters their function. Mounting evidence suggests that the addictive effects
of nicotine, like other drugs of abuse, occur through interactions with its receptors
in the mesolimbic dopamine system, particularly ventral tegmental area (VTA) neurons,
where nicotinic receptors act to modulate the release of dopamine. The molecular identity
of the nicotinic receptors responsible for drug seeking behavior, their cellular and
subcellular location and the mechanisms by which these receptors initiate and maintain
addiction are poorly defined. In this commentary, we review how nicotinic acetylcholine
receptors (nAChRs) are upregulated by nicotine exposure, the potential posttranslational
events that appear to cause it and how upregulation is linked to nicotine addiction.