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Relaxin-3/RXFP3 system regulates alcohol-seeking
Philip J. Ryan, Hanna E. Kastman, Elena V. Krstew, K. Johan Rosengren, Mohammed Akhter Hossain, Leonid Churilov, John D. Wade, Andrew L. Gundlach and Andrew J. Lawrence
Proceedings of the National Academy of Sciences of the United States of America
Vol. 110, No. 51 (December 17, 2013), pp. 20789-20794
Published by: National Academy of Sciences
Stable URL: http://www.jstor.org/stable/23761632
Page Count: 6
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Relapse and hazardous drinking represent the most difficult clinical problems in treating patients with alcohol use disorders. Using a rat model of alcohol use and alcohol-seeking, we demonstrated that central administration of peptide antagonists for relaxin family peptide 3 receptor (RXFP3), the cognate receptor for the highly conserved neuropeptide, relaxin-3, decreased selfadministration of alcohol in a dose-related manner and attenuated cue- and stress-induced reinstatement following extinction. By comparison, RXFP3 antagonist treatment did not significantly attenuate self-administration or reinstatement of sucrose-seeking, suggesting a selective effect for alcohol. RXFP3 is densely expressed in the stress-responsive bed nucleus of the stria terminalis, and bilateral injections of RXFP3 antagonist into the bed nucleus of the stria terminalis significantly decreased self-administration and stress-induced reinstatement of alcohol, suggesting that this brain region may, at least in part, mediate the effects of RXFP3 antagonism. RXFP3 antagonist treatment had no effect on general ingestive behavior, activity, or procedural memory for lever pressing in the paradigms assessed. These data suggest that relaxin-3/RXFP3 signaling regulates alcohol intake and relapse-like behavior, adding to current knowledge of the brain chemistry of rewardseeking.
Proceedings of the National Academy of Sciences of the United States of America © 2013 National Academy of Sciences