The extracellular Ca++ -independent component of luteinzing hormone (LH) secretion is manifest under the steroidal conditions known to induce gonadotrophine-releasing hormone (GnRH) self-potentiation

Quartered pituitaries obtained from intact males or gonadectomized males and females (72h) ± estradiol (24h) and/or testosterone (72h) implants were perifused at 0.25 ml/minute with Ca++ -free medium at 37°C, and sequential effluent fractions collected every 10 minutes, in an attempt to determine if the steroidal conditions known to induce or prevent GnRH self-potentiation would activate or inhibit the extracellular Ca++ -independent component of luteinizing hormone (LH) secretion. Continuous infusions (4h) of 1nmol GnRH or 1µmol of phorbol 12-myristate 13-acetate (PMA) did not stimulate LH secretion from the pituitaries of castrated males, intact males, estradiol-treated intact males or ovariectomized females. In contrast, estradiol induced delayed (20-30 minutes), protein synthesis-dependent components of LH secretion in response to both GnRH and PMA from pituitaries of gonadectomized males and females. Implantation of testosterone capsules immediately following gonadectomy resulted in an inhibition of the estradiol- induced GnRH- and PMA-stimulated responses from pituitaries of castrated or ovariectomized animals. These results suggest that estradiol can induce extracellular Ca++ -independent components of LH secretion from pituitaries of gonadectomized animals; responses which depend on de novo protein synthesis and which could involve protein kinase C. Additionally, the effects of estradiol are prevented by testosterone, indicating that this component of LH secretion is only apparent under the steroidal conditions known to facilitate GnRH self-potentiation.

The extracellular Ca++ -independent component of luteinzing hormone (LH) secretion is manifest under the steroidal conditions known to induce gonadotrophine-releasing hormone (GnRH) self-potentiation

Quartered pituitaries obtained from intact males or gonadectomized males and females (72h) ± estradiol (24h) and/or testosterone (72h) implants were perifused at 0.25 ml/minute with Ca++ -free medium at 37°C, and sequential effluent fractions collected every 10 minutes, in an attempt to determine if the steroidal conditions known to induce or prevent GnRH self-potentiation would activate or inhibit the extracellular Ca++ -independent component of luteinizing hormone (LH) secretion. Continuous infusions (4h) of 1nmol GnRH or 1µmol of phorbol 12-myristate 13-acetate (PMA) did not stimulate LH secretion from the pituitaries of castrated males, intact males, estradiol-treated intact males or ovariectomized females. In contrast, estradiol induced delayed (20-30 minutes), protein synthesis-dependent components of LH secretion in response to both GnRH and PMA from pituitaries of gonadectomized males and females. Implantation of testosterone capsules immediately following gonadectomy resulted in an inhibition of the estradiol- induced GnRH- and PMA-stimulated responses from pituitaries of castrated or ovariectomized animals. These results suggest that estradiol can induce extracellular Ca++ -independent components of LH secretion from pituitaries of gonadectomized animals; responses which depend on de novo protein synthesis and which could involve protein kinase C. Additionally, the effects of estradiol are prevented by testosterone, indicating that this component of LH secretion is only apparent under the steroidal conditions known to facilitate GnRH self-potentiation.