These authors contributed equally to this study.
Vasopressin 1a receptor knockout mice have a subtle olfactory deficit but normal aggression
Article first published online: 27 SEP 2006
No claim to original US government works
Genes, Brain and Behavior
Volume 6, Issue 6, pages 540–551, August 2007
How to Cite
Wersinger, S. R., Caldwell, H. K., Martinez, L., Gold, P., Hu, S.-B. and Young, W. S. (2007), Vasopressin 1a receptor knockout mice have a subtle olfactory deficit but normal aggression. Genes, Brain and Behavior, 6: 540–551. doi: 10.1111/j.1601-183X.2006.00281.x
- Issue published online: 27 SEP 2006
- Article first published online: 27 SEP 2006
- Received 7 July 2006, revised 7 September 2006, accepted for publication 12 September 2006
- agonistic behavior;
- circadian rhythm;
- social behavior
Two receptors for vasopressin (Avp) are expressed in the brain, the Avp 1a receptor (Avpr1a) and the Avp 1b receptor (Avpr1b). To investigate the role of Avpr1a in behaviors in mice more extensively, we generated a line of mice lacking a functional Avpr1a (knockout, Avpr1a−/−). We first performed a baseline phenotypic screen of the Avpr1a knockouts followed by a more detailed analysis of their circadian rhythms and olfactory function. When free-running in constant darkness, the Avpr1a−/− mice have a longer circadian tau than the wild types. There are also subtle olfactory deficits in Avpr1a−/− mice as measured in an olfactory habituation/dishabituation test and in the discrimination of female urine from male urine using an operant testing paradigm. An extensive body of research has shown that manipulation of the Avpr1a alters behavior, including aggression and social recognition. Therefore, we expected profound behavioral deficits in mice lacking the Avpr1a gene. Contrary to our expectations, social aggression, anxiety-like behavior and social recognition are unaffected in this line of Avpr1a knockout mice. These data suggest either that the Avpr1a is not as critical as we thought for social behavior in mice or, more likely, that the neural circuitry underlying aggression and other social behaviors compensates for the life-long loss of the Avpr1a. However, the olfactory deficits observed in the Avpr1a−/− mice suggest that Avp and Avpr1a drugs may affect behavior, in part, by modulation of chemosensory systems.