Abstract

Neonatal treatment with monosodium glutamate (MSG) induces severe neurochemical damage to several brain regions, and these lesions are expressed in adult life by a variety of endocrine and behavioral abnormalities. The present study analyzes the extent of the neurochemical damage to several monoaminergic systems by evaluating the changes in norepinephrine (NE), dopamine (DA), and 5-hydroxytryptamine (5-HT) metabolism induced by the neurotoxin in several discrete hypothalamic loci. Moreover, the study also evaluated the ability of MSG-treated rats to respond to acute ether stress, by measuring the release of ACTH and prolactin induced by ether and correlating those changes with the alterations in monoamine metabolism in the arcuate (AN), dorsomedial (DMN), and suprachiasmatic (SCN) nuclei and in the median eminence (ME). The results indicate that MSG treatment induces marked changes in monoamine metabolism in several of the regions examined. The metabolite of DA, dihydroxyphenylacetic acid, was markedly depressed in the AN, SCN, and DMN. NE metabolism was also significantly lower in the AN of MSG-treated animals. 5-HT metabolism was also altered by MSG treatment, with significant decrements recorded in the SCN, DMN, and AN. Both control and MSG-treated rats showed highly significant increments in ACTH and PRL release 5 and 15 min after exposure to ether vapors. The only quantitative difference between the two groups was a smaller increment in ACTH levels 5 min after ether in the MSG group. Ether stress increased DA metabolism in the AN, NE metabolism in the AN and DMN, and 5-HT metabolism in the SCN in control animals. With the exception of the latter, all these changes in amine metabolism were also observed in the MSG rats. In addition, increased NE and DA metabolism was recorded in the SCN and DMN of MSG-treated rats. The results indicate that although MSG treatment causes severe changes in amine metabolism in discrete brain regions, neither the neurochemical nor the hormone response to ether stress appears to be greatly affected. The additional changes in monoamine metabolism observed in MSG rats after ether may represent part of a compensatory mechanism evoked by the central nervous system in adaptation to the neonatally-induced neurochemical deficits.

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