RESUMO
We studied the sites of prolactin inhibition upon FSH-iniduced ovarian steroidogenesis and the ability of prolactin (Prl) to inhibit the synthesis of estradiol and cAMP accumulation under the stimulation of FSH or cAMP-dependent activators. The participation of other signal pathways such as PKC and Gi proteins on the inhibitory actions of Prl was also investigated using calfostine C and pertusis toxin as inhibitors. Results showed a dose-dependent prolactin decrease in FSH-induced estradiol and cAMP production prior and after the generation of the cyclic nucleotide by a mechanisn involving the catalytic subunit of adeniyl cyclase and/or through activation of PKC or by the interaction with pertusin toxin-sensitive G proteins. Our results suggest a mechanism by which G protein-coupled receptors are linked with those coupled with tyrosine kinase through the involvement of a Gi protein mediated mechanism.