The control of testicular androgen production in the goldfish: Effects of activators of different intracellular signalling pathways
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abstract
The putative roles of different signal transduction pathways in the regulation of testicular androgen production in goldfish were investigated. In addition to the role of the gonadotropin-adenylate cyclase pathway, which was studied using human chorionic gonadotropin and forskolin, we determined the effects of changes in intracellular calcium content and protein kinase C activation on androgen production using calcium ionophore A23187 and phorbol 12-myristate 13-acetate (PMA), respectively. Testis fragments incubated in vitro respond to hCG in a time- and dose-dependent manner with a resultant increase in the secretion of testosterone (T) and 11-ketotestosterone (11-KT). Although ineffective alone, PMA (400 nM) and A23187 (4000 nM) stimulate a small but significant increase (3-fold above basal) in T production. This response is minor compared to the up to 200-fold increase in T secretion observed in response to either hCG or forskolin. PMA (25-400 nM) alone and A23187 (250-4000 nM) alone inhibit the stimulatory actions of hCG on T production. Unlike PMA, the inactive phorbol 4 alpha-phorbol didecanoate, which does not activate PKC, had no effect on hCG-stimulated T production. PMA and A23187 did not influence the effects of forskolin on T production, suggesting that the compounds exert their effects prior to adenylate cyclase activation. In summary, the present studies suggest that in addition to the stimulatory actions of the adenylate cyclase second messenger system, changes in intracellular calcium content and protein kinase C activation may modulate testicular androgen production in the goldfish.
