Citation

Avegno EM, Salling MC, Borgkvist A, Mrejeru A, Whitebirch AC, Margolis EB, Sulzer D, Harrison NL. Neuropharmacology 2016; 110(Pt A): 386-395.

Affiliation

Department of Pharmacology, College of Physicians and Surgeons, Columbia University, New York, NY 10032, United States; Department of Anesthesiology, College of Physicians and Surgeons, Columbia University, New York, NY 10032, United States. Electronic address: nh2298@columbia.edu.

Copyright

(Copyright © 2016, Elsevier Publishing)

DOI

10.1016/j.neuropharm.2016.07.031

PMID

27475082

Abstract

Enhanced dopamine (DA) neurotransmission from the ventral tegmental area (VTA) to the ventral striatum is thought to drive drug self-administration and mediate positive reinforcement. We examined neuronal firing rates in slices of mouse midbrain following adolescent binge-like alcohol drinking and find that prior alcohol experience greatly enhanced the sensitivity to excitation by ethanol itself (10-50 mM) in a subset of ventral midbrain DA neurons located in the medial VTA. This enhanced response after drinking was not associated with alterations of firing rate or other measures of intrinsic excitability. In addition, the phenomenon appears to be specific to adolescent drinking, as mice that established a drinking preference only after the onset of adulthood showed no change in alcohol sensitivity. Here, we demonstrate that, not only does drinking during adolescence induce enhanced alcohol sensitivity, but that this DA neuronal response occurs over a range of alcohol concentrations associated with social drinking in humans.

Copyright © 2016. Published by Elsevier Ltd.

Language: en