Gonadotropin Releasing Hormone Inhibitory Autofeedback by Subproducts Antagonist at N-Methyl-D-Aspartate Receptors: A Model of Autocrine Regulation of Peptide Secretion
[en] The secretion of Gonadotropin-releasing Hormone (GnRH) involves activation of N-methyl-D-aspartate (NMDA) receptors. Here, we show that pulsatile GnRH secretion from hypothalamic explants is suppressed by 1-5GnRH, an endogenous breakdown product of GnRH, while 2-10GnRH has no effect. GnRH secretion evoked by NMDA is selectively inhibited by 1-5GnRH and this effect is similar to that of AP-5, a competitive antagonist at NMDA receptors. In addition, 1-5GnRH accounts for a dose-related inhibition of tritiated glutamate binding to hypothalamic membrane preparations. Using GnRH secretion as a model of NMDA-receptor controlled system, the effect of different peptides has been studied. Growth Hormone Releasing Factor (GRF), Insulin-like Growth Factor-I (IGF-I) and Proinsulin result in inhibition of GnRH secretion. Bioactive subproducts of those peptides (1-29GRF, 4-701GF-I and insulin) do not show any effect, suggesting that their classical receptors are not involved. In contrast, GnRH secretion is inhibited by other subproducts (1-37GRF, 1-31GF-I and C-peptide) all terminating in a glutamate residue. These subproducts selectively suppress the NMDA-evoked secretion of GnRH. Protease inhibitors prevent the inhibitory effects of IGF-I on GnRH secretion. This, breakdown products of different peptide hormones are possible endogenous antagonists at NMDA receptors. This effect could account for an autocrine or paracrine limitation of NMDA-receptor-mediated secretion of peptides.
Disciplines :
Endocrinology, metabolism & nutrition
Author, co-author :
Bourguignon, Jean-Pierre ; Université de Liège - ULiège > Département des sciences cliniques > Pédiatrie
Alvarez Gonzalez, Maria-Luz ; Université de Liège - ULiège > Département des sciences cliniques > Labo de biologie des tumeurs et du développement
Gerard, Arlette ; Centre Hospitalier Universitaire de Liège - CHU > Pédiatrie
Franchimont, P.
Language :
English
Title :
Gonadotropin Releasing Hormone Inhibitory Autofeedback by Subproducts Antagonist at N-Methyl-D-Aspartate Receptors: A Model of Autocrine Regulation of Peptide Secretion
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Bibliography
Bourguignon JP, Gérard A, Franchimont P 1989 Direct activation of GnRH secretion through different receptors to neuroexcitatory amino acids. Neuroendocrinology 49:402-408
Bourguignon JP, Gérard A, Mathieu J, Simons J, Franchimont P 1989 Pulsatile release of gonadotropin releasing hormone from hypothalamic expiants is restrained by blockade of N-methyl-D, L aspartate receptors. Endocrinology 125:1090-1096
Bourguignon JP, Gérard A, Alvarez Gonzalez ML, Franchimont P 1992 Neuroendocrine mechanism of onset of puberty: sequential reduction in activity of inhibitory and facilitatory N-Methyl-D-Aspartate receptors. J Clin Invest 90:1736-1744
Mahachoklertwattana P, Sanchez J, Grumbach MM, Kaplan SL, Rosenthal SM 1993 N-Methyl-D-Aspartate (NMDA) stimulates LHRH release via the NMDA receptor in an LHRH neuronal cell line (GT-1). Ped Res 33(suppl), pS34 (abstr)
Bourguignon, JP, Gérard A, Franchimont P 1990 Maturation of the hypothalamic control of pulsatile gonadotropin-releasing hormone at onset of puberty. II. Reduced potency of an inhibitory autofeedback. Endocrinology 127:2884-2890
Krause JE, Advis JP, McKelvy JF 1982 Characterization of the site of cleavage of Luteinizing Hormone-releasing hormone under conditions of measurement in which LHRH degradation undergoes physiologically related change. Biochem Biophys Res Commun 108: 1475-1481
Sandberg AC, Engberg C, Lake M, Van Holst H, Sara VR 1988 The expression of insulin-like growth factor I and insulin-like growth factor II genes in the human fetal and adult brain and in glioma. Neurosci Lett 93:114-119
Bourguignon, JP, Gérard A, Alvarez Gonzalez ML, Franchimont P 1993 Acute suppression of Gonadotropin-releasing Hormone secretion by Insulin-like Growth Factor-I and subproducts: an age-dependent endocrine effect. Neuroendocrinology, 58:525-530
Harrisson NL, Simmonds MA 1985 Quantitative studies on some antagonists of NMDA in slices of rat cerebral cortex. Br J Pharmacol 84:381-391
Merriam GR, Wachter KW 1982 Algorithms for the study of episodic hormone secretion. Am J Physiol 249:E310-E318
Foster AC, Wong EHF 1987 The novel anticonvulsivant MK-801 binds to the activated state of the N-methyl-D-aspartate receptor in rat brain. Br J Pharmacol 91:403-409
Bourguignon JP, Gérard A, Alvarez Gonzalez ML, Fawe L, Franchimont P 1992 Gonadal-independent developmental changes in activation of N-methyl-D-aspartate receptors involved in gonadotropin-releasing hormone secretion. Neuroendocrinology 55:634-641
Cotman CW, Monaghan DT, Ottersen OP, Storm-Mathisen J 1987 Anatomical organization of excitatory amino acid receptors and their pathways. Trends Neurosci 10:273-280
Sasaki A, Sato S, Yumita S, Hanew K, Miura Y, Yoshinaga K 1989 Multiple forms of immunoreactive Growth hormone-releasing hormone in human plasma, hypothalamus, and tumor tissues. J Clin Endocrinol Metab 68:180-185
Sara V, Carlsson-Skwirut C, Andersson C, Hall E, Sjdren B, Holmgren A, Jornvall H 1986 Characterization of somatomedins from human fetal brain: identification of a variant form of insulin-like growth factor I. Proc Natl Acad Sci USA 83:4904-4907
Steiner DF, Cho S, Oyer PE, Terris S, Peterson JD, Rubinstein AH 1971 Isolation and characterization of proinsulin C-peptide from bovine pancreas. J Biol Chem 246:1365-1374
Griffiths EC, Hopkinson CRN 1979 Inactivation of two hyperactive LHRH analogues by rat hypothalamic peptidases. Hormone Res 10:233-242
Rothman SL, Olney JW 1987 Excitotoxicity and the NMDA receptor. Trends Neurosci 10:299-302
Gluckman PD, Klempt N, Guan J, Mallard C, Sirimanne E, Drager-now M, Klempt M, Singh K, Williams C, Nikolics K 1992 A role for IGF-I in the rescue of CNS neurons following hypoxic-ischemic injury. Biochem Biophys Res Commun 182:593-599
Gluckman PD, Guan J, Williams C, Bielharz E, Sirimanne E, Klempt N 1992 The role of insulin-like growth factor-I (IGF-1) in central neuronal rescue in "The role of insulin-like growth factors in the nervous system". Arlington, VA, pl8 (abstr)
Bertrand G, Gross R, Puech R, Loubatieres-Mariani MM, Bockaert J 1992 Evidence for a glutamate receptor of the AMPA subtype which mediates insulin release from rat perfused pancreas. Br J Pharmacol 106:354-359
Wojeikowski C, Blackman J, Ostrega D, Lewis G, Galloway J, Rubenstein AH, Polonsky KS 1990 Lack of effect of high-dose biosynthetic human C-peptide on pancreatic hormone release in normal subjects. Metabolism, 39:827-832
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