title: Effect of neonatal treatment with monosodium glutamate on dopaminergic and L-DOPA-ergic neurons of the medial basal hypothalamus and on prolactin and MSH secretion of rats.
abstract: The effect of neonatal treatment with monosodium L-glutamate (MSG) on the dopaminergic systems of the medial basal hypothalamus has been investigated using tyrosine hydroxylase (TH) and aromatic L-amino acid decarboxylase (AADC) immunocytochemistry. Changes in plasma levels of prolactin (PRL) and alpha-melanocyte-stimulating hormone (MSH) have also been determined in intact and in MSG-treated rats after inhibition of TH by alpha-methyl-p-tyrosine (alpha-MpT) or without inhibition of enzyme activity. Monosodium glutamate resulted in a 40% reduction in the number of TH immunopositive tuberoinfundibular neurons, but no change in the number of AADC-positive tuberoinfundibular nerve cells, indicating that this reduction has occurred mainly in TH-positive but AADC-negative elements, i.e., in L-DOPA-ergic neurons. In contrast, MSG did not cause changes in the number of TH and AADC immunoreactive neurons of the periventriculohypophysial and tuberohypophysial dopaminergic systems, and it did not influence basal plasma PRL levels. alpha-methyl-p-tyrosine has increased plasma PRL concentrations in both control and MSG-treated rats of both sexes, but significantly higher responses were detected in females. None of the treatments had any effect on plasma MSH level. These findings suggest that MSG affects primarily L-DOPA-ergic neurons located in the ventrolateral part of the arcuate nucleus, but not dopaminergic neurons situated in the dorsomedial part of the arcuate nucleus; neither PRL nor MSH secretion is altered by MSG; a significant sex difference exists in the pituitary PRL response to inhibition of TH, and this response is not affected by MSG.
authors.affiliation: Neuroendocrine Research Laboratory, Department of Human Morphology and Developmental Biology, Semmelweis University, Budapest, Hungary.
authors.forename: I
authors.initials: I
authors.lastname: Bodnár
authors.forename: P
authors.initials: P
authors.lastname: Göõz
authors.forename: H
authors.initials: H
authors.lastname: Okamura
authors.forename: B E
authors.initials: BE
authors.lastname: Tóth
authors.forename: M
authors.initials: M
authors.lastname: Vecsernyé
authors.forename: B
authors.initials: B
authors.lastname: Halász
authors.forename: G M
authors.initials: GM
authors.lastname: Nagy
mesh_terms: D000818:Animals; D000831:Animals, Newborn / Q000033:anatomy & histology / Q000254:growth & development / Q000378:metabolism; D001111:Arcuate Nucleus of Hypothalamus / Q000187:drug effects* / Q000201:enzymology / Q000254:growth & development; D001142:Aromatic-L-Amino-Acid Decarboxylases / Q000378:metabolism; D002452:Cell Count; D004298:Dopamine / Q000378:metabolism*; D004791:Enzyme Inhibitors / Q000494:pharmacology; D005260:Female; D007150:Immunohistochemistry; D007980:Levodopa / Q000378:metabolism*; D008297:Male; D009074:Melanocyte-Stimulating Hormones / Q000097:blood / Q000187:drug effects* / Q000378:metabolism; D009474:Neurons / Q000187:drug effects* / Q000201:enzymology / Q000378:metabolism; D009498:Neurotoxins / Q000494:pharmacology; D011388:Prolactin / Q000097:blood / Q000187:drug effects* / Q000378:metabolism; D051381:Rats; D017207:Rats, Sprague-Dawley; D012098:Reproduction / Q000187:drug effects / Q000502:physiology; D012727:Sex Characteristics; D012970:Sodium Glutamate / Q000494:pharmacology*; D014446:Tyrosine 3-Monooxygenase / Q000037:antagonists & inhibitors / Q000378:metabolism; D019805:alpha-Methyltyrosine / Q000494:pharmacology
chemical_list: D004791:Enzyme Inhibitors; D009498:Neurotoxins; D007980:Levodopa; D019805:alpha-Methyltyrosine; D011388:Prolactin; D009074:Melanocyte-Stimulating Hormones; D014446:Tyrosine 3-Monooxygenase; D001142:Aromatic-L-Amino-Acid Decarboxylases; D004298:Dopamine; D012970:Sodium Glutamate