Abstract

We have developed an animal model for studying the effects of excessive prolactin release (hyperprolactinemia) on male reproductive and sexual functions. Transplantation of four pituitary glands under the kidney capsules of adult male rats produces a chronic significant elevation of circulating prolactin (PRL) levels, reduction in gonadotropin (LH & FSH) release, increase in testicular LH binding and deficits of copulatory behavior. We have already shown that effects of grafts on sexual behavior are due to PRL secreted by the grafts and that this effect is not mediated by stimulation of adrenal activity. We now propose to determine if deficits of copulatory behavior in hyperprolactinemic male rats can be corrected by administration of LHRH, testosterone or estradiol and whether pituitary grafts suppress mating behavior in gonadectomized animals treated with testosterone. In a series of studies in vivo and in vitro, we will compare testicular responsiveness to gonadotropins in hyperprolactinemic and control rats. Finally, we will study behavioral and hormonal correlates of very severe hyperprolactinemia induced by transplantation of PRL-producing tumors. The results should indicate by what mechanisms excessive PRL release can interfere with libido, potency and hormone production by the testes.

  Funding Agency

Agency
National Institute of Health (NIH)
Institute
Eunice Kennedy Shriver National Institute of Child Health & Human Development (NICHD)
Type
Research Project (R01)
Project #
5R01HD020001-02
Application #
3317751
Study Section
Reproductive Biology Study Section (REB)
Project Start
1984-07-01
Project End
1986-11-30
Budget Start
1984-12-01
Budget End
1985-11-30
Support Year
2
Fiscal Year
1985
Total Cost
Indirect Cost

  Institution

Name
Southern Illinois University Carbondale
Department
Type
Schools of Arts and Sciences
DUNS #
939007555
City
Carbondale
State
IL
Country
United States
Zip Code
62901

  Publications

Srivastava, Vinod K; Dearth, Robert K; Hiney, Jill K et al. (2002) Alcohol suppresses insulin-like growth factor-1 gene expression in prepubertal transgenic female mice overexpressing the bovine growth hormone gene. Alcohol Clin Exp Res 26:1697-702
Gonzalez, L; Miquet, J G; Sotelo, A I et al. (2002) Cytokine-inducible SH2 protein up-regulation is associated with desensitization of GH signaling in GHRH-transgenic mice. Endocrinology 143:386-94
Kinney, B A; Coschigano, K T; Kopchick, J J et al. (2001) Evidence that age-induced decline in memory retention is delayed in growth hormone resistant GH-R-KO (Laron) mice. Physiol Behav 72:653-60
Gonzalez, L; Sotelo, A I; Bartke, A et al. (2001) Growth hormone (GH) and estradiol regulation of membrane-associated GH binding protein and GH receptors in GH releasing hormone transgenic mice. Growth Horm IGF Res 11:34-40
Danilovich, N A; Bartke, A; Winters, T A (2000) Ovarian follicle apoptosis in bovine growth hormone transgenic mice. Biol Reprod 62:103-7
Gonzalez, L; Sotelo, A I; Bartke, A et al. (1999) Up-regulation of GH-binding protein by mouse GH in transgenic mice overexpressing GH-releasing hormone. J Endocrinol 163:299-307
Debeljuk, L; Steger, R W; Wright, J C et al. (1999) Effects of overexpression of growth hormone-releasing hormone on the hypothalamo-pituitary-gonadal function in the mouse. Endocrine 11:171-9
Matthews, J C; Beveridge, M J; Dialynas, E et al. (1999) Placental anionic and cationic amino acid transporter expression in growth hormone overexpressing and null IGF-II or null IGF-I receptor mice. Placenta 20:639-50
Bartke, A; Chandrashekar, V; Turyn, D et al. (1999) Effects of growth hormone overexpression and growth hormone resistance on neuroendocrine and reproductive functions in transgenic and knock-out mice. Proc Soc Exp Biol Med 222:113-23
Dialynas, E; Brown-Borg, H; Bartke, A (1999) Immune function in transgenic mice overexpressing growth hormone (GH) releasing hormone, GH or GH antagonist. Proc Soc Exp Biol Med 221:178-83

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