To explore the involvement of pituitary progesterone receptor (PR) in basal and stimulated LH secretion and in luteinizing hormone releasing hormone (LHRH) self-priming elicited through PKC signalling pathway and the role of the oestrogen (E) environment, eight randomly selected hemipituitaries from adult female rats in pro-oestrus or from 2 weeks ovariectomized (OVX) rats under ether anaesthesia were incubated, in the absence of P, over 3 h in DMEM. In the first experiment, hemipituitaries were incubated continuously with: medium alone, LHRH (10 nM), the PKC stimulator phorbol ester 12-myristate 13-acetate (PMA; 100 nM), LHRH + the PKC inhibitor staurosporine (100 nM), LHRH+RU486 (10 nM) and PMA+RU486. Control pituitaries were incubated with staurosporine or RU486. In the second experiment, hemipituitaries from control rats in pro-oestrus or OVX rats were incubated, 1 h apart, with LHRH to determine the LHRH self-priming and this was compared with the priming effect of PMA. Also, the effect of staurosporine and RU486 on LHRH self-priming and PMA priming was studied. Medium was aspirated every hour to determine LH accumulation in the medium and LHRH self-priming. Rats were humanely killed.

Both LHRH and PMA stimulated LH secretion; staurosporine reduced basal and LHRH-stimulated LH secretion and RU486 reduced basal and LHRH- and PMA-stimulated LH secretion from proestrous pituitaries. The stimulating effect of LHRH and PMA on LH secretion was significantly reduced in OVX rats. Both LHRH and PMA induced LHRH priming. Staurosporine reduced LHRH self-priming while RU486 reduced both LHRH self-potentiation and PMA priming. The magnitude of these effects was blunted in OVX rats. These results indicated that the PKC signalling pathway in the gonadotrope mediated basal and LHRH-stimulated LH secretion and LHRH self-priming in an oestrogen-dependent manner through ligand-independent activation of PR.