Literature DB >> 7413022

Monosodium glutamate disruption of behavioral and endocrine function in the female rat.

J F Rodriguez-Sierra, R Sridaran, C A Blake.   

Abstract

Experiments were conducted to determine the effects of neonatal administration of L-monosodium glutamate (MSG) on behavioral and endocrine function in the female rat. Administration of MSG (4 mg/kg body weight) at days 1, 3, 5, 7 and 9 in neonates results in a delay of vaginal opening (VO) and the absence of ovulation at the time of VO. However, some rats were observed to ovulate after VO if they were subjected to sequential laparotomies. MSG-treated rats also fail to exhibit compensatory ovarian hypertrophy. Ovariectomized MSG-treated rats injected with estradiol benzoate (EB) followed by a progesterone injected 2 days later did not exhibit sexual beahvior to male rats, while all the control rats displayed lordosis. Chronic treatment with EB for 12 days, followed by a progesterone injection on the 12th day, resulted in a marked improvement of the sexual receptivity of the MSG-treated rats. The body weight of the MSG-treated animals was lower than that of the controls during development although the MSG animals looked obese. Food intake is normal in the MSG-treated rats, but when expressed as intake/100 g body weight, the MSG-treated rats appeared slightly hyperphagic, MSG-treated rats respond with increased food intake after ovariectomy and EB treatment suppresses the increased food intake. Thus, the control of food intake by estrogen does not seem to be affected by the MSG treatment; in fact, these animals seem to be more sensitive than control rats to the anorectic effects of EB. Neonatal MSG treatment appears to affect the neural control for the tonic secretion of gonadotropins by destroying arcuate nuclei. This undoubtedly reduces the reproductive capacity of the animals by impeding the growth and secretions of their ovaries. The findings that chronic estrogen followed by progesterone treatment can reinstate sexual receptivity in MSG-treated animals suggests that the arcuate nuclei are not needed for the expression of sexual behavior and that estrogens might remedy the fertility problems of MSG-treated animals.

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Year:  1980        PMID: 7413022     DOI: 10.1159/000123079

Source DB:  PubMed          Journal:  Neuroendocrinology        ISSN: 0028-3835            Impact factor:   4.914


  6 in total

1.  A decrease of cytosol estrogen receptors in the hypothalamus as a result of treatment of neonatal rats with glutamate.

Authors:  J F Rodriguez-Sierra; J D Blaustein; C A Blake; R W Clough; K A Elias
Journal:  Exp Brain Res       Date:  1982       Impact factor: 1.972

2.  Depopulation of the ventromedial hypothalamic nucleus in the diabetic Chinese hamster.

Authors:  D R Garris; A R Diani; C Smith; G C Gerritsen
Journal:  Acta Neuropathol       Date:  1982       Impact factor: 17.088

3.  Neonatal monosodium glutamate treatment counteracts circadian arrhythmicity induced by phase shifts of the light-dark cycle in female and male Siberian hamsters.

Authors:  Brian J Prendergast; Kenneth G Onishi; Irving Zucker
Journal:  Brain Res       Date:  2013-05-20       Impact factor: 3.252

4.  Monosodium glutamate-induced lesions in the rat cingulate cortex.

Authors:  K Rascher
Journal:  Cell Tissue Res       Date:  1981       Impact factor: 5.249

Review 5.  Glutamate in the mammalian CNS.

Authors:  S Sahai
Journal:  Eur Arch Psychiatry Clin Neurosci       Date:  1990       Impact factor: 5.270

6.  Cross-fostering reduces obesity induced by early exposure to monosodium glutamate in male rats.

Authors:  Rosiane Aparecida Miranda; Claudinéia Conationi da Silva Franco; Júlio Cezar de Oliveira; Luiz Felipe Barella; Laize Peron Tófolo; Tatiane Aparecida Ribeiro; Audrei Pavanello; Ellen Paula Santos da Conceição; Rosana Torrezan; James Armitage; Patrícia Cristina Lisboa; Egberto Gaspar de Moura; Paulo Cezar de Freitas Mathias; Elaine Vieira
Journal:  Endocrine       Date:  2016-04-26       Impact factor: 3.633

  6 in total

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