This proposal is a further examination of the mechanism by which immobilization stress inhibits the testicular response to gonadotropin in male rats. Experiments will focus on the transmission of the stress signal to the testis, mediation (pituitary, adrenal, immune system and gonadal) of the stress effect on the testis, effect of stress on the LH transducing system in Leydig cells and identification of site or sites of the inhibitory lesion in the steroidogenic pathway. A second series of experiments will further investigate the role of proopiomelanocortin peptides (pituitary, immune system, and gonadal origin), CRH, glucocorticoids and angiotensin II (Ag II) in attenuating testicular steroid production during stress. The effect of stress on the dynamics of LH/HCG binding, the adenyl cyclase system, Gi unit, changes in intracellular calcium (Leydig cell populations and single cell; spectrofluorometry and image analysis), and protein kinase C activation in Leydig cells will be examined in the third series of experiments. We will further examine the site(s) of the stressed-induced lesion in the steroidogenic pathway. The effect of stress and regulators of stress responses on enzymes involved in cholesterol synthesis and mobilization, and the synthesis and metabolism of T will be investigated. These experiments will define the mechanism of stress-induced testicular hyposensitivity to gonadotropin, and the role that pituitary, immune and gonadal regulatory factors play in this process.
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