Depletion of hypothalamic growth hormone-releasing hormone by neonatal monosodium glutamate treatment reveals an inhibitory effect of betamethasone on growth hormone secretion in adult rats

Roger Corder, Patrick Soudan, Musalnah Mazlan, Charles McLean, Rolf C. Gaillard

Research output: Contribution to journalArticle

18 Citations (Scopus)

Abstract

Rats were treated with monosodium glutamate (MSG), 4 mg/g on alternate days for the first 10 days of life, to induce lesions of the arcuate nucleus and destroy the majority of growth hormone-releasing hormone (GHRH) neurones. At 10 weeks of age, control (n = 42) and MSG-treated (n = 36) male rats were used to test the effect of glucocorticoids on growth hormone (GH) secretion. Each treatment group was divided into six study groups to determine the effect of betamethasone (BM), administered either 3 or 20 h prior to sacrifice, alone and in combination with hypoglycaemia (insulin 0.1 U/100 g). BM treatment of male rats was without effect on plasma GH levels in control animals. In contrast, glucocorticoid administered either 3 h before sacrifice or the previous evening significantly reduced circulating GH (p <0.001) in MSG-treated animals. The difference in plasma GH response to BM pretreatment in control rats and those with lesions of the arcuate nucleus indicates a hypothalamic action of glucocorticoids, presumably on somatostatin and GHRH neurones. In control animals the effects appear to be counterbalancing, but following destruction of GHRH neurones an uncompensated inhibitory influence was observed. Male MSG-treated rats had lower body weight (-25%) and reduced hypothalamic GHRH (-89%) and pituitary GH content (-69%) compared to male controls. Female rats which had undergone the same neonatal MSG treatment (n = 40) when sacrificed I week after their male counterparts showed similar reductions in body weight (-15%), hypothalamic GHRH (-74%), and pituitary GH (-67%). Interestingly, the hypothalamic concentration of GHRH in control female rats (n = 39) was only 41% of male controls, suggesting an important effect of sex hormones on GHRH neurones.

Original languageEnglish
Pages (from-to)85-92
Number of pages8
JournalNeuroendocrinology
Volume51
Issue number1
DOIs
Publication statusPublished - 1990
Externally publishedYes

Fingerprint

Hypothalamic Hormones
Betamethasone
Growth Hormone-Releasing Hormone
Sodium Glutamate
Growth Hormone
Glucocorticoids
Neurons
Arcuate Nucleus of Hypothalamus
Body Weight
Gonadal Steroid Hormones
Somatostatin
Hypoglycemia
Insulin

Keywords

  • Arcuate nucleus
  • Glucocorticoid
  • Glucocorticoid receptor
  • Growth
  • Growth hormone-releasing hormone
  • Somatostatin

ASJC Scopus subject areas

  • Endocrinology
  • Endocrinology, Diabetes and Metabolism
  • Cellular and Molecular Neuroscience
  • Endocrine and Autonomic Systems
  • Neuroscience(all)

Cite this

Depletion of hypothalamic growth hormone-releasing hormone by neonatal monosodium glutamate treatment reveals an inhibitory effect of betamethasone on growth hormone secretion in adult rats. / Corder, Roger; Soudan, Patrick; Mazlan, Musalnah; McLean, Charles; Gaillard, Rolf C.

In: Neuroendocrinology, Vol. 51, No. 1, 1990, p. 85-92.

Research output: Contribution to journalArticle

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abstract = "Rats were treated with monosodium glutamate (MSG), 4 mg/g on alternate days for the first 10 days of life, to induce lesions of the arcuate nucleus and destroy the majority of growth hormone-releasing hormone (GHRH) neurones. At 10 weeks of age, control (n = 42) and MSG-treated (n = 36) male rats were used to test the effect of glucocorticoids on growth hormone (GH) secretion. Each treatment group was divided into six study groups to determine the effect of betamethasone (BM), administered either 3 or 20 h prior to sacrifice, alone and in combination with hypoglycaemia (insulin 0.1 U/100 g). BM treatment of male rats was without effect on plasma GH levels in control animals. In contrast, glucocorticoid administered either 3 h before sacrifice or the previous evening significantly reduced circulating GH (p <0.001) in MSG-treated animals. The difference in plasma GH response to BM pretreatment in control rats and those with lesions of the arcuate nucleus indicates a hypothalamic action of glucocorticoids, presumably on somatostatin and GHRH neurones. In control animals the effects appear to be counterbalancing, but following destruction of GHRH neurones an uncompensated inhibitory influence was observed. Male MSG-treated rats had lower body weight (-25{\%}) and reduced hypothalamic GHRH (-89{\%}) and pituitary GH content (-69{\%}) compared to male controls. Female rats which had undergone the same neonatal MSG treatment (n = 40) when sacrificed I week after their male counterparts showed similar reductions in body weight (-15{\%}), hypothalamic GHRH (-74{\%}), and pituitary GH (-67{\%}). Interestingly, the hypothalamic concentration of GHRH in control female rats (n = 39) was only 41{\%} of male controls, suggesting an important effect of sex hormones on GHRH neurones.",
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