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NEURONAL‐GLIAL CONTRIBUTIONS TO TRANSMITTER AMINO ACID METABOLISM: STUDIES WITH KAINIC ACID‐INDUCED LESIONS OF RAT STRIATUM
Author(s) -
NICKLAS W. J.,
Nunez R.,
Berl S.,
Duvoisin R.
Publication year - 1979
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.1471-4159.1979.tb09913.x
Subject(s) - glutamine , glutamate receptor , kainic acid , striatum , biochemistry , medicine , kainate receptor , metabolism , endocrinology , glutamic acid , chemistry , biology , amino acid , dopamine , ampa receptor , receptor
– Various aspects of amino acid metabolism were studied in striatum of rats with unilateral, kainic acid‐induced lesions. Tissue slices were prepared from the lesioned and the contralateral, unlesioned, striatum. The preparations were incubated with a mixture of d ‐[2‐ 14 C]glucose and [ 3 H]acetate in a Krebs‐Ringer bicarbonate medium to evaluate oxidative metabolism. Glutamate and aspartate levels were decreased in the slices prepared from the lesioned striata by 35‐40% and that of GABA by 75% compared to the levels found in the slices from the contralateral striata; glutamine levels were not different in the two preparations. Glucose utilization was decreased 60% in the slices from the lesioned striatum; this was caused not only by decreased levels of glutamate, aspartate and GABA but also by a decreased rate of labelling of glutamate and aspartate. On the other hand, the metabolism of [ 3 H]acetate was greatly increased. The specific activities of glutamate and aspartate were 4‐5‐fold higher in the slices from kainic acid‐lesioned striata; those of glutamine and GABA were unchanged. Thus, there was a 6‐7‐fold increase in the ratio of 3 H to 14 C in the specific activities of glutamate, aspartate and GABA with no change in this ratio in glutamine. The labelling of glutamine relative to that of glutamate, especially from [ 3 H]acetate, suggested that the compartmentation of the glutamate‐glutamine system was greatly altered in the kainate‐lesioned striatum which now more closely resembled a single compartment system. The activities of lactate dehydrogenase, glutamate dehydrogenase, GABA transaminase and ‘cytoplasmic’ aspartate aminotransferase were decreased in homogenates of lesioned striatum. Succinate dehydrogenase, glutaminase (phosphate‐activated) and ‘mitochondrial’ aspartate aminotransferase activities were unchanged whilst that of glutamine synthetase was increased. The results are consistent with hypotheses concerning the assignment of labelled acetate metabolism to glial cells as well as the distribution of the above enzymes between glia, neurones and nerve endings.