R. Baldessarini, C. Yorke
Oct 1, 1974
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Journal
Journal of Neurochemistry
Abstract
—The uptake of l[14C]glutamine by a crude isolated nerve ending fraction of rat brain was found to be linear with time for at least 5 min, profoundly temperature‐dependent, apparently half‐saturated at a substrate concentration of 0·26 mm, partially inhibited by dinitrophenol and ouabain and elevated [K+], weakly Na+‐dependent, poorly inhibited by drugs which block uptake of biogenic amines and more strongly inhibited by glutamic acid (IC50= 0·5mm) than by aspartic acid, GABA, glycine or methionine. The [14C]glutamine taken up appeared to be associated with nerve endings and was released by membrane‐disruption; about 20 per cent was associated with free mitochondria. Glutamine, δ‐aminolevulinic acid and several other amino acids were poor inhibitors of [3H]GABA‐uptake; δ‐aminolevulinic acid was a poor inhibitor of [3H]glutamine‐uptake, whereas glutamine was a moderately effective competitive inhibitor (Ki= 1 mm). [14C]glutamine and [3H]GABA were released from brain slices by electrical stimulation or 50 mm K+, while labeled δ‐aminolevulinic acid, leucine, urea, amphetamine and tyramine were poorly released. [14C]glutamine was not released by unlabeled glutamate or several aromatic amines. We conclude that the neuropsychiatric features of porphyria are not likely due to a ‘false transmitter’ role for δ‐aminolevulinic acid although such a role for glutamine in hepatic encephalopathy or other neuropsychiatric diseases should be considered.