Pituitary adenylate cyclase-activating polypeptide induces testicular testosterone synthesis through PGE2 mediation in crested newt, Triturus carnifex

The aim of the present work was to study the possible role of adenylate cyclase-activating polypeptide (PACAP) 38 in the testicular intracellular mechanism regulating steroidogenesis of crested newt, Triturus carnifex. Gonads were incubated in vitro with PACAP 38 and prostaglandin (PG) E2 alone or with inhibitors of cyclooxygenase (COX), adenylate cyclase (AC), and phospholipase C (PLC) for 30 min and 60 min. PGE2, PGF2α, testosterone, and estradiol-17β were measured in the culture medium; aromatase (AR) activity and cAMP were assessed in the tissue. PACAP 38 increased PGE2 (30 min and 60 min), estradiol-17β (60 min), cAMP (60 min), and AR (60 min) but decreased testosterone (60 min). PGE2 increased estradiol-17β, cAMP, and AR and decreased testosterone at 30 and 60 min.PLC inhibitor counteracted the effects of PACAP 38, while AC inhibitor counteracted these effects except for PGE2 increase. AC inhibitor counteracted the effects of PGE2, while PLC did not. COX inhibitor decreased PGF2α (30 min and 60 min), PGE2 (30 min and 60 min), estradiol-17β (60 min), cAMP (60 min), and AR (60 min), but increased testosterone (60 min). These in vitro results suggest that, in newt testis, PACAP 38 acts on PLC, inducing the increase of PGE2 which, in turn, acting on AC, increases AR activity with the consequent estradiol-17β increase and testosterone decrease.