Behavioral study shows adolescent nicotine increases morphine reward in adults, suggesting long-term neural disruptions.
The idea that nicotine exposure during adolescence increases the likelihood of later opioid use has sat at the crossroads of epidemiology and neuroscience for decades. Behavioral studies in humans and in animals have consistently hinted at this, but only recently has the field begun to uncover the underlying mechanisms. In the current issue of Biological Psychiatry , Wittenberg et al. ( 1 ) provide a compelling cellular explanation for how adolescent nicotine alters the brain’s response to opioids long after the nicotine itself is gone. Through an elegant integration of behavioral assays, ex vivo electrophysiology, and chemogenetics, the authors show that nicotine exposure during adolescence reorganizes inhibitory signaling in the ventral tegmental area (VTA) in a manner that later enhances morphine reward in adults.
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Hollon et al. (2026) studied this question.
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