Vasopressin V1b receptor knockout reduces aggressive behavior in male mice

UMMS Affiliation

Department of Pediatrics; Brudnick Neuropsychiatric Research Institute, Department of Psychiatry

Publication Date


Document Type



Age Factors; Aggression; Animals; Behavior, Animal; Body Temperature; Brain Chemistry; Corticosterone; Eating; Exploratory Behavior; Female; Male; Maze Learning; Mice; Mice, Inbred C57BL; Mice, Knockout; Motor Activity; Neurons; Phenotype; Proto-Oncogene Proteins c-fos; Receptors, Vasopressin; Recognition (Psychology); Sexual Behavior, Animal; Stress, Physiological; Testosterone; Visual Perception


Neurology | Pediatrics | Psychiatry


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. We suggest that V1bR antagonists could prove useful for treating aggressive behavior seen, for example, in dementias and traumatic brain injuries.

DOI of Published Version



Mol Psychiatry. 2002;7(9):975-84. Link to article on publisher's site

Journal/Book/Conference Title

Molecular psychiatry

Related Resources

Link to Article in PubMed

PubMed ID