Increased vulnerability to cocaine in mice lacking the serotonin-1B receptor

Beatriz A. Rocha, Kimberly Scearce-Levie, José J. Lucas, Noboru Hiroi, Nathalie Castanon, John C. Crabbe, Eric J. Nestler and René Hen ()
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Beatriz A. Rocha: University of North Texas Health Science Center
Kimberly Scearce-Levie: Center for Neurobiology and Behavior, Columbia University
José J. Lucas: Center for Neurobiology and Behavior, Columbia University
Noboru Hiroi: Laboratory of Molecular Psychiatry, Yale University School of Medicine
Nathalie Castanon: Center for Neurobiology and Behavior, Columbia University
John C. Crabbe: Department of Veterans Affairs Medical Center and Oregon Health Sciences University
Eric J. Nestler: Laboratory of Molecular Psychiatry, Yale University School of Medicine
René Hen: Center for Neurobiology and Behavior, Columbia University

Nature, 1998, vol. 393, issue 6681, 175-178

Abstract: Abstract There is increasing evidence that genetic factors can influence individual differences in vulnerability to drugs of abuse1,2. Serotonin (5-hydroxytryptamine, 5-HT), acting through many receptors can modulate the activity of neural reward pathways and thus the effects of various drugs of abuse3,4,5,6,7,8. Here we examine the effects of cocaine in mice lacking one of the serotonin-receptor subtypes, the 5-HT1B receptor9. We show that mice lacking 5-HT1B display increased locomotor responses to cocaine and that they are more motivated to self-administer cocaine. We propose that even drug-naive 5-HT1B-knockout mice are in a behavioural and biochemical state that resembles that of wild-type mice sensitized to cocaine by repeated exposure to the drug. This altered state might be responsible for their increased vulnerability to cocaine.

Date: 1998
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DOI: 10.1038/30259

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