Larrea F, Sánchez-González S, García-Becerra R, Méndeza I

Language: Spanish
References: 28
Page: 259-266
PDF size: 133.39 Kb.

ABSTRACT

We studied the sites of prolactin inhibition upon FSH-induced 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 mechanism involving the catalytic subunit of adenyl 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.

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