Treatment implications: using neuroscience to guide the development of new pharmacotherapies for alcoholism

Abstract

Developing pharmacotherapies to treat alcohol dependence and associated health problems traditionally has been based on gaining a better understanding of the neuroscience underlying alcohol-drinking behavior. To date, three medications have been approved for the treatment of alcohol dependence: disulfiram (Antabuse®), naltrexone (Revia®, Vivitrol®, and Naltrel®), and acamprosate (Campral®). However, these medications have modest efficacy, and there is a great need for newer medications that target different neurochemical systems and which could be used either as adjunctive treatments or to treat subpopulations of drinkers. Furthermore, it also is important to improve current treatment options by understanding and incorporating differences in how people with certain genes respond to medication (i.e., pharmacogenetic differences).

Figure

Medications and their proposed sites of action on the neural pathways that have been shown to mediate alcohol reinforcement. CB1 = cannabi-noid-1, CRF = corticotrophin-releasing factor, GABA = γ-aminobutyric acid, NA = nucleus accumbens, NK1 = neurokinin 1, VTA = ventral tegmental area.