For years, researchers have known smoking represents a risk factor for later alcohol abuse; however, the mechanisms underlying this link have long remained a mystery. Now, researchers reporting in the Cell Press journal Neuron believe they may have finally uncovered the source for this enigmatic relationship.
In a study conducted in rats, the scientists showed that even a single exposure to nicotine temporarily changed how the reward system in the creatures' brains responded to alcohol, increasing the reinforcing properties of it via stress hormones.
As this happened, the rats exposed to nicotine sought to drink more alcohol than their peers.
Furthermore, signaling in the brain's reward system was dampened when the nicotine-exposed animals consumed alcohol.
This decreased reward response to alcohol arose via two mechanisms: an initial activation of stress hormone receptors and a subsequent rise in inhibitory signaling in the brain.
Both of these processes, the researchers found, were responsible for causing the rats to self-administer more alcohol after nicotine exposure.
"Our findings indicate the mechanisms by which nicotine influences the neural systems associated with alcohol abuse, providing a foundation for conceptualizing strategies aimed at diminishing the link between smoking and later alcohol abuse," senior author Dr. John Dani, of the Baylor College of Medicine said in a press release.
In doing so, Dani argues, researchers could be helping to lower the rate of alcohol abuse among those who take up smoking early in their lives.
"Young people typically experiment with nicotine from tobacco in their teens, and that exposure possibly contributes to a greater vulnerability to alcohol abuse later in life. Therefore, greater vigilance is called for to prevent the initial exposure to nicotine and to follow those at risk," he said. "In addition, our work suggests that stress hormones are candidate targets for prevention or treatment therapies."