Neonatal monosodium glutamate treatment abolishes both delta opioid receptor-induced and alpha-2 adrenoceptor-mediated gastroprotection in the lower brainstem in rats

Neonatal monosodium glutamate treatment reduced immunoreactive beta-endorphin content in the mediobasal hypothalamus by 50% in adult, male Wistar rats as compared to hypertonic saline-treated littermates; there was also a moderate (approx. 25%) reduction in the rostral part of the nucleus of the sol...

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Bibliographic Details
Published in:Journal of physiology, Paris Paris, 2001, Vol.95 (1), p.215-220
Main Authors: Rónai, András Z, Gyires, Klara, Barna, István, Müllner, Katalin, Palkovits, Miklós
Format: Article
Language:English
Subjects:
(D-Ala 2, D-Leu 5)-enkephalin
Adrenergic alpha-Agonists - pharmacology
Animals
Animals, Newborn - physiology
beta-Endorphin - antagonists & inhibitors
beta-Endorphin - metabolism
Brain Stem - drug effects
Brain Stem - physiology
Clonidine
Clonidine - pharmacology
Cytoprotection - drug effects
Enkephalin, Leucine-2-Alanine - pharmacology
Gastroprotection
Growth - drug effects
Male
Monosodium glutamate
Neurotransmitter Agents - metabolism
Pupil - radiation effects
Rats
Rats, Wistar
Receptors, Adrenergic, alpha - physiology
Receptors, Opioid, delta - physiology
Sodium Glutamate - pharmacology
Stomach - physiology
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Summary:Neonatal monosodium glutamate treatment reduced immunoreactive beta-endorphin content in the mediobasal hypothalamus by 50% in adult, male Wistar rats as compared to hypertonic saline-treated littermates; there was also a moderate (approx. 25%) reduction in the rostral part of the nucleus of the solitary tract. In sham-treated adults the intracisternally injected alpha-2 adenoceptor stimulant clonidine (0.47 nmol/rat) and the delta opioid receptor type agonist (D-Ala 2, D-Leu 5)-enkephalin (0.8 nmol/rat) reduced acidified ethanol-induced mucosal lesions in the stomach by 84.1 and 77.5%, respectively, whereas the same doses were completely ineffective in rats treated neonatally by monosodium glutamate. The data taken together with the results of previous studies with the same substances in rats with retroarcuate knifecuts suggest that neuronal damage in the nucleus of the solitary tract region rather than in the arcuate nucleus is responsible for the changes seen in the pharmacological responsiveness.
ISSN:0928-4257
1769-7115
DOI:10.1016/S0928-4257(01)00028-6