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Effect of Cortico‐Striate Pathway Lesion on the Activities of Enzymes Involved in Synthesis and Metabolism of Amino Acid Neurotransmitters in the Striatum
Author(s) -
Sandberg M.,
Ward H. K.,
Bradford H. F.
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.tb07110.x
Subject(s) - glutaminase , glutamine synthetase , striatum , glutamate receptor , glutamate dehydrogenase , glutamine , biology , lesion , glutamate decarboxylase , medicine , endocrinology , malate dehydrogenase , enzyme , biochemistry , amino acid , dopamine , pathology , receptor
The activities of several enzymes involved in the metabolism of aspartate and glutamate were measured in striatal (nucleus caudatus and putamen) homogenates 2–3, 6–7, and 35–40 days following frontoparietal and frontal cortical ablation. The activity of glutamine synthetase (GS) was substantially increased (46–48%) on the operated side 6–7 days following the lesion whereas smaller changes were observed at 2–3 and 35–40 days after lesion. In contrast, decreased levels of glutaminase and malate dehydrogenase (MDH) were observed by 6–7 days while no significant change was found at either 2–3 or 35–40 days after the lesion. The activities of glutamate dehydrogenase (GDH) and glutamate decarboxylase (GAD) were elevated after 35–40 days whereas no changes in the levels of either GDH or aspartate aminotransferase (ASAT) were found at 2–3 or 6–7 days after the fronto‐parietal decortication. When only the frontal cortex was removed quantitatively similar changes were observed in striatal GS and glutaminase activity. The content of glutamate and glutamine in the denervated striatum followed qualitatively the changes in glutaminase and GS. The results indicate that the degeneration of cortico‐striatal terminals causes a profound glial reaction in the striatum, and both glutaminase and MDH are present in relatively high concentrations in the corticostriatal terminals.