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The Journal of Neuroscience, June 17, 2009, 29(24):7658-7666; doi:10.1523/JNEUROSCI.1311-09.2009

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Behavioral/Systems/Cognitive
Adult Testosterone Treatment But Not Surgical Disruption of Vomeronasal Function Augments Male-Typical Sexual Behavior in Female Mice

Kristine L. Martel and Michael J. Baum

Department of Biology, Boston University, Boston, Massachusetts 02215

Correspondence should be addressed to Dr. Michael J. Baum, Department of Biology, Boston University, 5 Cummington Street, Boston, MA 02215. Email: baum{at}bu.edu

It was recently reported that female mice lacking a functional vomeronasal organ (VNO) displayed male-typical sexual behavior indiscriminately toward female and male conspecifics. These results have been cited as showing that a circuit controlling male-typical sex behavior exists in both sexes, with its activation in females being tonically inhibited by VNO signaling, independent of adult sex hormones. We further assessed this hypothesis while controlling the endocrine status of female mice in which VNO function was surgically disrupted. In experiment 1, VNO-lesioned (VNOx) female mice showed no more mounting or pelvic-thrusting behavior toward an estrous female or a castrated, urine-swabbed male (presented simultaneously) than sham-operated (VNOi) females. This was true when subjects were either ovary-intact or ovariectomized and treated with estradiol, estradiol plus progesterone, or testosterone. In experiment 2, female mice given accessory olfactory bulb lesions or a sham lesion displayed equivalent frequencies of male sex behaviors when given testosterone after ovariectomy. In experiment 3, VNOx and VNOi females displayed equivalent frequencies of male sex behaviors toward an estrous female or a castrated male (presented in separate tests), again, when given testosterone after ovariectomy. Our results confirm early reports that adult testosterone can stimulate appreciable male-typical sex behavior in female mice. However, we failed to corroborate the recent claim that VNO signaling normally inhibits the activity of neural circuitry controlling the expression of male-typical mating behavior by female mice.

Received March 17, 2009; revised April 21, 2009; accepted May 4, 2009.

Correspondence should be addressed to Dr. Michael J. Baum, Department of Biology, Boston University, 5 Cummington Street, Boston, MA 02215. Email: baum{at}bu.edu


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