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A genetic basis for aggression and anger

ARTICLE 1: "Vasopressin V1b receptor knockout reduces aggressive behavior in male mice"

AUTHORS: SR Wersinger, EI Ginns, AM O'Carroll, SJ Lolait, WS Young III

Section on Neural Gene Expression, NIMH, Bethesda, MD, USA; Brudnick Neuropsychiatric Research Institute, University of Massachusetts Medical School, Worcester, MA, USA; University Research Centre For Neuroendocrinology, University of Bristol, UK

Increased aggression is commonly associated with many neurological and psychiatric disorders. Current treatments are largely empirical and are often accompanied by severe side effects, underscoring the need for a better understanding of the neural bases of aggression. Vasopressin, acting through its 1a receptor subtype, is known to affect aggressive behaviors. The vasopressin 1b receptor (V1bR) is also expressed in the brain, but has received much less attention due to a lack of specific drugs. Here we report that mice without the V1bR exhibit markedly reduced aggression and modestly impaired social recognition. By contrast, they perform normally in all the other behaviors that we have examined, such as sexual behavior, suggesting that reduced aggression and social memory are not simply the result of a global deficit in sensorimotor function or motivation. Fos-mapping within chemosensory responsive regions suggests that the behavioral deficits in V1bR knockout mice are not due to defects in detection and transmission of chemosensory signals to the brain. The authors suggest that V1bR antagonists could prove useful for treating aggressive behavior seen, for example, in dementias and traumatic brain injuries.

Citation source: Molecular Psychiatry 2002 Volume 7, number 9, pages 975-984.

For further information on this work, please contact Dr. W. Scott Young III, NIMH, Bldg. 36, Room 2A11, MSC 4068, Bethesda, MD 20892-4068, USA. Phone: 301-496-8767; FAX: 301-402-6473; E-mail: scott@co
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Contact: Aimee Midei
molecularpsychiatry@mednet.ucla.edu
310-206-6739
Molecular Psychiatry
4-Nov-2002


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