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THE METABOLISM OF [ 14 C]GLUCOSE BY THE BRAINS OF SUCKLING RATS INTOXICATED WITH INORGANIC LEAD
Author(s) -
Patel A. J.,
Michaelson I. A.,
Cremer J. E.,
Balázs R.
Publication year - 1974
Publication title -
journal of neurochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.75
H-Index - 229
eISSN - 1471-4159
pISSN - 0022-3042
DOI - 10.1111/j.1471-4159.1974.tb06898.x
Subject(s) - glutamine , forebrain , medicine , endocrinology , cerebellum , glutamate receptor , amino acid , biology , cerebral cortex , glutamic acid , metabolism , citric acid cycle , labelling , lead acetate , biochemistry , central nervous system , chemistry , toxicity , receptor
—The development with age of the pattern of distribution of glucose carbon characteristic of the adult brain was studied in 7‐, 13‐, 19‐ and 24‐day‐old rats suckling from mothers maintained on a diet containing 4·5% lead acetate or on a normal diet. In normal rats the rapid and extensive conversion of glucose carbon into amino acids associated with the tricarboxylic acid cycle has been shown to develop in the cerebellum and the cerebral cortex during the same period as previously observed for the whole forebrain. A significant retardation was observed in both brain parts of rats suckling from mothers ingesting lead. In comparison with glutamate, aspartate and γ‐aminobutyrate, the labelling of glutamine was particularly low. The concentration of glutamine was not affected in the forebrain, but it was elevated in the cerebellum. The age‐dependent rise in the amounts of glutamate and aspartate was also retarded, but it would appear that the contribution of this effect to the depressed labelling of amino acids was small. There was no evidence of impaired entry of glucose into the brain from the blood. Although in comparison with undernourished animals, the growth retardation of the lead‐treated rats is similar, several of the effects observed on the developing brain seem to be distinct.