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Glucose and Synaptosomal Glutamate Metabolism: Studies with [ 15 N]Glutamate
Author(s) -
Erecińska Maria,
Zaleska Malgorzata M.,
Nissim Itzhak,
Nelson David,
Dagani Fiorenzo,
Yudkoff Marc
Publication year - 1988
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.1471-4159.1988.tb01826.x
Subject(s) - glutamate receptor , metabolism , chemistry , carbohydrate metabolism , biochemistry , glutamic acid , neuroscience , endocrinology , biology , amino acid , receptor
The metabolism of [ 15 N]glutamate was studied with gas chromatography‐mass spectrometry in rat brain synaptosomes incubated with and without glucose. [ 15 N]‐Glutamate was taken up rapidly by the preparation, reaching a steady‐state level in <5 min. 15 N was incorporated predominantly into aspartate and, to a much lesser extent, into γ‐aminobutyrate. The amount of [ 15 N]ammonia formed was very small, and the enrichment of 15 N in alanine and glutamine was below the level of detection. Omission of glucose substantially increased the rate and amount of [ 15 N]aspartate generated. It is proposed that in synaptosomes (a) the predominant route of glutamate nitrogen disposal is through the aspartate aminotransferase reaction; (b) the aspartate aminotransferase pathway generates 2‐oxoglutarate, which then serves as the metabolic fuel needed to produce ATP; (c) utilization of glutamate via transami‐nation to aspartate is greatly accelerated when flux through the tricarboxylic acid cycle is diminished by the omission of glucose; (d) the metabolism of glutamate via glutamate de‐hydrogenase in intact synaptosomes is slow, most likely reflecting restriction of enzyme activity by some unknown factors), which suggests that the glutamate dehydrogenase reaction may not be near equilibrium in neurons; and (e) the activities of alanine aminotransferase and glutamine synthetase in synaptosomes are very low.