A genetic basis for aggression and anger

November 04, 2002

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@codon.nih.gov

ARTICLE 2: "Association of anger-related traits with SNPs in the TPH gene"

AUTHORS: D Rujescu, I Giegling, B Bondy, A Gietl, P Zill, HJ Möller

Molecular Neurobiology, Ludwig-Maximilians-University, Munich, Germany; Department of Psychiatry, Ludwig-Maximilians-University, Munich, Germany

Since both aggression-related traits and serotonergic activity are partially heritable and correlate inversely, variations in genes of the serotonergic system might then, to some extent, account for variations in aggression-related behavior. Tryptophan hydroxylase (TPH) is the rate limiting biosynthetic enzyme in the serotonin pathway and regulates levels of serotonin. Recently, a genetic variation in TPH has been associated with aggression and anger-related traits in volunteers. We investigated a sample of community-based healthy volunteers (n = 154) and suicide attempters (n = 86), a clinical population with a high risk for elevated impulsive aggression and related traits. The subjects were genotyped for an A218C and an A779C single nucleotide polymorphism (SNP) located in the TPH gene. All subjects were administered standard psychiatric interviews as well as self-report questionnaires for aggression, irritability and anger-related traits. For anger-related traits, a multivariate effect of the tryptophan hydroxylase genotype and an interaction effect for genotype and diagnosis was observed in healthy volunteers and suicide attempters after controlling for age and educational level. U-carriers in both groups showed higher scores for State Anger, Trait Anger and Angry Temperament. These findings support the hypothesis that the A218C and the A779C SNP in the TPH gene may be associated with anger-related traits in German samples.

Citation source: Molecular Psychiatry 2002 Volume 7, number 9, pages 1023-1029.

For further information on this work, please contact Dr. Dan Rujescu, Molecular Neurobiology, Department of Psychiatry, Ludwig-Maximilians-University, Nussbaumstr 7, D-80336 Munich, Germany. Phone: 49-89-5160-5756; E-mail: Dan.Rujescu@psy.med.uni-muenchen.de

Molecular Psychiatry is published by the Nature Publishing Group. http://www.nature.com/mp

Editor: Julio Licinio, M.D.; phone: 310-825-7113; FAX: 310-206-6715; e-mail: licinio@ucla.edu

For a copy of these articles, please contact Aimee Midei, editorial assistant, e-mail: molecularpsychiatry@mednet.ucla.edu.

PLEASE CITE MOLECULAR PSYCHIATRY AS THE SOURCE OF THIS MATERIAL.
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Molecular Psychiatry

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