Abstract
Several steps of cAMP- and substrate-dependent testosterone production in the testes were studied with laboratory mouse micropopulations of six inbred strains (A/He, CBA/Lac, C57Bl/6J, DD, YT, PP). The strains differed in basal testosterone production in the gonads and in its response to activation of the adenylate cyclase signal transduction pathway at various steps by human chorionic gonadotropin (hCG), the cholera toxin, forskolin, and dibutyryl-cAMP and in the presence of pregnenolone, an early precursor of testosterone. Establishment of dominant–subordinate relationships in mouse populations substantially affected testosterone production in response to all activators of testicular steroidogenesis. The secretory activity of the testes decreased at the early establishment of social hierarchy in experimental micropopulations, then returned to the initial level, and again decreased in the case of activation with hCG, dibutyryl-cAMP, and pregnenolone. With all activators of steroidogenesis, basal and activated testosterone production changed in the same direction during the establishment and maintenance of social hierarchy, suggesting coordinated changes in all examined steps of testosterone biosynthesis in the testes. The among-strain differences in response to all activators of steroidogenesis remained much the same at various stages of the establishment of social hierarchy. The parameters of cAMP- and substrate-dependent testosterone production averaged over individual stages of the establishment of social hierarchy proved associated. Their genotypic correlations were positive and, in many cases, significant. Subsequent component analysis showed that one principal component accounted for more than 80% of the total among-strain variation, suggesting a coordinated genetic control of the endocrine function of the testes.
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Busygina, T.V., Osadchuk, A.V. The Effects of the Genotype and Social Stress on cAMP- and Substrate-Dependent Mechanism Regulating the Hormone-Producing Function of Mouse Testes. Russian Journal of Genetics 37, 528–534 (2001). https://doi.org/10.1023/A:1016670732482
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DOI: https://doi.org/10.1023/A:1016670732482