Journal of Andrology
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Published-Ahead-of-Print March 19, 2009, DOI:10.2164/jandrol.108.007443

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Normal Responses to Restraint Stress in Mice Lacking the Gene for Neuronal Nitric Oxide Synthase

Ben Avi Weissman , Chantal M. Sottas , Michael Holmes , Ping Zhou , Costantino Iadecola , Dianne Hardy , Ren-Shan Ge *, and Matthew P. Hardy

* To whom correspondence should be addressed. E-mail: rge{at}popcbr.rockefeller.edu.

The hormonal changes associated with immobilization stress (IMO) include a swift increase in corticosterone (CORT) concentration and a decrease in circulating testosterone (T) levels. There is evidence that the production of the short lived neuromodulator nitric oxide (NO) is increased during stress in various tissues, including the brain. NO also suppresses the biosynthesis of T. Both the inducible and the neuronal isoforms of NO synthase (i- and nNOS, respectively) have been implicated in this suppression, but the evidence has not been conclusive. We used adult wild type (WT) and nNOS knockout male mice (nNOS-/-) to assess the respective roles of CORT and nNOS-derived NO in stress mediated inhibition of T production. Animals were assigned to either basal control or 3 h IMO groups. No difference in basal plasma and testicular T levels were observed between WT and nNOS-/-, although testicular weights of mutant mice were slightly lower compared to WT animals. The plasma content of luteinizing hormone (LH) and CORT in unstressed mice of both genotypes were similar. Exposure to 3 h of IMO increased plasma CORT and decreased T concentrations in mice of both genotypes. However, comparable levels of plasma LH and testicular nitrite and nitrate (NOx), NO stable metabolites, were detected in control and stressed WT and nNOS-/- mice. Adrenal concentrations of NOx declined after IMO, but the reduction was not statistically significant. These findings implicate CORT rather than NO generated by nNOS in the rapid stress-induced suppression of circulating testosterone.


Key words: Androgen • Reproductive Tract • Steroidogenesis • Testis • Stress • nNOS null mice






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