Addictive Nicotine and Stress Induce Convergent Mechanisms That Increase Alcohol Self‐administration

About this Seminar

Addictive drug reinforcement and stress signaling involve common neural circuitry. Dr. Dani and his team demonstrated in rodents that pre-exposure to nicotine or stress attenuates alcohol-induced dopamine responses and increases alcohol self-administration. A blunted dopamine signal results from ethanol-induced GABAergic excitation of GABA neurons in the ventral tegmental area. Blocking stress hormone receptors or preventing excitatory GABA signaling prevented the attenuated alcohol-induced dopamine response and prevented the increased alcohol self-administration caused by nicotine or stress. These results demonstrate that nicotine and stress alter the neural and behavioral responses to alcohol through a neuroendocrine signal that shifts inhibitory GABA transmission towards excitation.

Additional Details

This is a free event hosted by the Fralin Biomedical Research Institute and co-sponsored by the institute's Center for Human Neuroscience Research. The Pioneers in Biomedical Research Seminar Series, which runs annually from September to May, has featured leading biomedical researchers from throughout the country since the program began in 2012. The lectures are also open to all members of the Virginia Tech community including graduate students, undergraduates, faculty, and staff, as well as the public.

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