The long-term objectives are to elucidate neuroendocrine control mechanisms involved in anterior pituitary gland (APG) luteinizing hormone (LH) and follicle-stimulating hormone (FSH) secretion. Studies are designed to determine the importance of LH releasing hormone (LHRH), the hypothalamus, and the gonads on the differentiation, development and maintenance of gonadotropin secretion in both sexes and the importance of interrelationships between prolactin (PRL) and LH/FSH secretion. More specifically, studies are expected to show that LHRH is needed for the differentiation of LH cells and the differentiation of FSH in LH cells, LH cells but not FSH cells will be maintained in the chronic absence of LHRH; LHRH controls the percentage of gonadotropes which contain LH or LH and FSH as well as the percentage of APG cells which are gonadotropes (GTS); some sex differences in GTS are due to neonatal androgenization and others are maintained by circulating steroids; increases in serum LH and FSH levels after castration are due to increases in the basal LH and FSH release rates, the LH and fSH increments of GTS in response to LHRS, and hyperplasia and hypertrophy of GTS; an inverse relationship exists between the number of GTS and the number PRL cells; PRL has a suppressive effect on FSH release; and the anatomical cellular proximity of GTS and PRL cells is important to the control of LH, FSH and PRL secretion. These goals will be achieved by employing the following techniques in rats and/or mice: radioimmunoassay of LH, FSH, PRL, LHRH, estrogen, progesterone and testosterone; incubation of anterior pituitaries in culture medium; transplantation of pituitary glands beneath the renal capsule; collection of serial blood samples in cannulated rats; immunocytochemical staining of LH, FSH and PRL cells for examination and morphometric determinations at the light and electron microscope levels; administration of phenobarbital, synthetic LHRH, estrogen, progesterone, testosterone or dihydrotestosterone to rats; and employment of dwarf mice and rat pars tuberalis tissue which lack PRL. These studies will result in significant contributions to our knowledge of the neuroendocrine control mechanisms for LH, FSH and PRL secretion in health and disease. The ability to alter LH, FSH and PRL cell numbers has particular potential clinical applications with regard to fertility, sterility, and PRL adenomas.

National Institute of Health (NIH)
Eunice Kennedy Shriver National Institute of Child Health & Human Development (NICHD)
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Reproductive Biology Study Section (REB)
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University of South Carolina at Columbia
Schools of Medicine
United States
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Blake, C A; Nair-Menon, J U; Campbell, G T (1997) Estrogen can protect splenocytes from the toxic effects of the environmental pollutant 4-tert-octylphenol. Endocrine 6:243-9
Boockfor, F R; Blake, C A (1997) Chronic administration of 4-tert-octylphenol to adult male rats causes shrinkage of the testes and male accessory sex organs, disrupts spermatogenesis, and increases the incidence of sperm deformities. Biol Reprod 57:267-77
Blake, C A; Boockfor, F R (1997) Chronic administration of the environmental pollutant 4-tert-octylphenol to adult male rats interferes with the secretion of luteinizing hormone, follicle-stimulating hormone, prolactin, and testosterone. Biol Reprod 57:255-66
Nair-Menon, J U; Campbell, G T; Blake, C A (1996) Toxic effects of octylphenol on cultured rat and murine splenocytes. Toxicol Appl Pharmacol 139:437-44
Campbell, G T; Gore, A C; Woller, M J et al. (1996) Adenohypophysial allografts releasing prolactin decrease prolactin mRNA concentration in the host hamster's adenohypophysis in situ. Neuroendocrinology 63:430-6
Woller, M J; Campbell, G T; Blake, C A (1996) Changes in percentages of adenohypophysial gonadotrophs associated with the sex-specific, selective increase in serum follicle-stimulating hormone concentration in the juvenile female hamster. Biol Reprod 54:800-8
Woller, M J; Campbell, G T; Blake, C A (1995) Neuropeptide Y and luteinizing hormone releasing hormone synergize to stimulate the development of cellular follicle-stimulating hormone in the hamster adenohypophysis. J Neuroendocrinol 7:733-6
Woller, M J; Campbell, G T; Blake, C A (1995) Induction of cellular follicle-stimulating hormone in the hamster adenohypophysis requires intermittent stimulation by luteinizing hormone releasing hormone. J Neuroendocrinol 7:393-400
Augustine, J R; Mascagni, F; McDonald, A J et al. (1993) Immunocytochemical staining of neuropeptide Y (NPY) in the insular lobe of the monkey: a light microscopic study. Brain Res 603:255-63
Woller, M J; Campbell, G T; Liu, L et al. (1993) Estrogen alters the effects of neuropeptide-Y on luteinizing hormone and follicle-stimulating hormone release in female rats at the level of the anterior pituitary gland. Endocrinology 133:2675-81

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