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

• 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
• ISSN: 0928-4257; 1769-7115
• DOI: 10.1016/S0928-4257(01)00028-6

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.