Review
eCollection 2015 Sep.How Menthol Alters Tobacco-Smoking Behavior: A Biological Perspective
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- PMCID: PMC4553648
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Review
How Menthol Alters Tobacco-Smoking Behavior: A Biological Perspective
R J Wickham. Yale J Biol Med..
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Abstract
Mentholated cigarettes gained popularity in the 1950s and were often marketed as "healthy" cigarettes, attributable to their pleasurable mint flavor and cooling sensation in the mouth, lungs, and throat. While it is clear that nicotine is the primary psychoactive component in tobacco cigarettes, recent work has suggested that menthol may also play a role in exacerbating smoking behavior, despite original health claims. Recent evidence highlights four distinct biological mechanisms that can alter smoking behavior: 1) menthol acts to reduce the initially aversive experiences associated with tobacco smoking; 2) menthol can serve as a highly reinforcing sensory cue when associated with nicotine and promote smoking behavior; 3) menthol's actions on nicotinic acetylcholine receptors may change the reinforcing value of nicotine; and 4) menthol can alter nicotine metabolism, thus increasing nicotine bioavailability. The purpose of this review is to highlight and evaluate potential biological mechanisms by which menthol can alter smoking behavior.
Keywords: acetylcholine; addiction; menthol; nicotine; stobacco cigarettes.
Figures
Schematic how menthol can modulate phasic DA release in VTA and NAc. a) Presynaptic VTA nAChRs: Presynaptic α7 nAChR are expressed predominately on glutamate terminals in the VTA. Menthol’s actions here may be to reduce cholinergic and nicotinic activation of presynaptic α7 nAChRs, thus producing less glutamate and resulting in less burst-firing and phasic DA release [69]. Menthol acting on α4β2* nAChRs on GABA terminals may have the effect of decreasing inhibitory tone on DA neurons, relieving them from inhibition and increasing burst-firing and phasic DA release. In contrast, menthol acting on excitatory presynaptic α4β2* nAChRs on cholinergic terminals would decrease acetylcholine release elicited by nicotine and result in less burst-firing and phasic DA release.b) Somatodendritic VTA nAChRs: Somatodendritic expression of α4β2* and α6β2* nAChRs expressed on DA cell bodies may produce less burst-firing and subsequent phasic DA release to nicotine when menthol is present, since menthol decreases nicotine’s efficacy at these receptors.c) Presynaptic NAc nAChRs: Menthol acting on presynaptic α6β2* nAChRs [70-72] located on DA terminals in the NAc would likely increase phasic DA release to DA neuron burst-firing, since menthol is effectively serving as an antagonist at this receptor.
Potential biological mechanisms that can explain observed smoking behavior differences between menthol and non-menthol smokers.
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