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Methionine‐Induced Changes in Glutamate, Aspartate, Glutamine, and γ‐Aminobutyrate Levels in Brain Tissue
Author(s) -
Wood J. D.,
Kurylo E.,
Geddes J. W.
Publication year - 1985
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.1471-4159.1985.tb04060.x
Subject(s) - glutamine , glutamate receptor , methionine , free nerve ending , synaptosome , glutamic acid , amino acid , biochemistry , biology , metabolism , glutamine synthetase , medicine , chemistry , endocrinology , central nervous system , receptor
Intramuscular administration of methionine to mice resulted in changes in the levels of aspartate, glutamate, glutamine, and γ‐aminobutyrate in both nerve endings (synaptosomes) and “non‐nerve‐ending” tissue in the brain. However, the amino acid changes in the two locations differed considerably, not only in the time to onset of the changes, but also in the direction of the changes and in their duration. The results provide additional support for a glutamate‐glutamine cycle between neurons and glia, and suggest that the decreases in amino acid levels in the nerve endings are due to an insufficient supply of glutamine from glia or other cellular structures, possibly compounded by an impairment in the uptake of glutamine into the nerve terminals. The primary cause of the glutamine deficiency is unknown because methionine did not affect the enzymes of glutamate and glutamine metabolism. Treatment of mice with methionine also resulted in an anticonvulsant action, but no correlation was observed between the latter phenomenon and the glutamate content of nerve endings.