In order to develop these needed medications, a better understanding of cocaine's brain mechanisms is required. Although it is known that cocaine acts on at least three different transporter systems -- the dopamine transporter, the serotonin transporter and the norepinephrine transporter -- it is not clear which combination of transporter systems holds the most potential as targets for developing treatments for cocaine abuse.
Recently, a collaborative research effort led by scientists at the University of North Carolina/Chapel Hill and Duke University used genetically-modified mice to provide information about the mediation of cocaine's rewarding effects. These findings promise to guide the development of potential medications for cocaine abuse. Drs. L.A. Dykstra, L.M. Bohn, R.M. Rodriguiz, W.C. Wetsel, R.R. Gainetdinov and M. G. Caron. University of North Carolina at Chapel Hill, Duke University, and Howard Hughes Medical Institute, presented their results at an American Society for Pharmacology & Experimental Therapeutics session at the Experimental Biology 2003 meeting in San Diego. In these studies, mice were genetically altered so they lacked two of the potential mediators of cocaine's effects. One of those mediators was the dopamine transporter, which is considered to be the primary site of cocaine's rewarding effects. The other mediator was the norepinephrine transporter.
Cocaine's rewarding effects were still apparent in mice that were lacking both the dopamine and the norepinephrine transporter. Indeed, cocaine was just as rewarding in mice lacking these targets as in control mice
Contact: Sarah Goodwin
Federation of American Societies for Experimental Biology