Abstract
Normal responses to restraint stress in mice lacking the gene for neuronal nitric oxide synthase
Weissman,Ben-Avi; Sottas,Chantal M.; Holmes,Michael; Zhou,Ping; Iadecola,Costantino; Hardy,Dianne O.; Ge,Renshan; Hardy,Matthew P.
Journal of Andrology 30(5): 614-620
Publication date: 2009
The hormonal changes associated with immobilization stress (IMO)include a swift increase in corticosterone (CORT) concentrationand a decrease in circulating testosterone (T) levels. Thereis evidence that the production of the short lived neuromodulatornitric oxide (NO) is increased during stress in various tissues,including the brain. NO also suppresses the biosynthesis ofT. 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 wildtype (WT) and nNOS knockout male mice (nNOS-/-) to assess therespective roles of CORT and nNOS-derived NO in stress mediatedinhibition of T production. Animals were assigned to eitherbasal control or 3 h IMO groups. No difference in basal plasmaand testicular T levels were observed between WT and nNOS-/-,although testicular weights of mutant mice were slightly lowercompared 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 Tconcentrations in mice of both genotypes. However, comparablelevels of plasma LH and testicular nitrite and nitrate (NOx),NO stable metabolites, were detected in control and stressedWT and nNOS-/- mice. Adrenal concentrations of NOx declinedafter IMO, but the reduction was not statistically significant.These findings implicate CORT rather than NO generated by nNOSin the rapid stress-induced suppression of circulating testosterone.
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