Growth hormone (GH ) cells may augment or influence gonadotropes during the estrous cycle to enhance fertility. Transitory cells with GH antigens that express LH and FSH-beta subunit mRNAs and antigens (in the same or separate storage granules) appear just before ovulation. Furthermore, they also bind analogs of gonadotropin releasing hormone (GnRH) and growth hormone releasing hormone (GHRH). These cells may be transitional somatogonadotropes that function to support ovulation. The hypothesis for aim 1 is that somatogonadotropes will express GH or prolactin mRNA and Pit-1 transcription factors and gonadotropin antigens during late diestrus and early proestrus. Furthermore, this expression may be stimulated by exposing cells from diestrous rats to estradiol, activin and/or GnRH. The somatogonadotropes will be detected by in situ hybridization for GH, Pit-1, LH, or FSH beta mRNAs followed by immunolabeling for the gonadotropin antigens. The second group of studies (Aim 2) will test the hypothesis that the transitional somatogonadotropes from proestrus rats can secrete LH or FSH. The assays will include the reverse hemolytic plaque assays, cell dot blot assays, and radioimmunoassays. Secretagogues for gonadotropes and somatotropes will also be used to learn if they affect secretion. Aim 3 studies will test the hypothesis that somatogonadotropes will increase expression of mRNA for GnRH receptors during diestrus and will maintain their ability to bind GHRH. This binding will be detected by affinity cytochemical protocols which use biotinylated analogs of the ligands to label target cells. Alternatively, GH may be present in gonadotropes as a regulatory molecule. Thus, aim 4 will test the hypothesis that GH may mediate gonadotrope functions during proestrus. Effects of exogenous and endogenous GH on gonadotropin secretion, storage, and synthesis will be tested. GH is now considered a co-gonadotropin because of its ability to enhance fertility in some patients. These studies will elucidate role(s) for GH during ovulation in the pituitary.

R01HD033915

1996-08-01

2003-05-31