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It was also decreased in acute kainic acid\u2010lesioned striatum where glutamate uptake was unaffected. Aspartate aminotransferase, however, decreased only after acute kainic acid treatment. Results for glutamate uptake, glutamate decarboxylase, and choline acetyltransferase were in agreement with previous findings. These results suggest that ornithine may act as a precursor for glutamate in nerve terminals, although the nonspecific localization does not allow ornithine aminotransferase to be a convenient biochemical marker. The decrease in aspartate aminotransferase is thought to be due to be widespread cell degeneration after acute kainic acid. Aspartate aminotransferase activities were also found to be reduced in the frontal cortex, caudate nucleus and putamen of Huntington's disease brains.<\/jats:p>","DOI":"10.1002\/jnr.490080408","type":"journal-article","created":{"date-parts":[[2005,1,1]],"date-time":"2005-01-01T10:11:13Z","timestamp":1104574273000},"page":"643-650","source":"Crossref","is-referenced-by-count":12,"title":["Effects of kainic acid injection and cortical lesion on ornithine and aspartate aminotransferases in rat striatum"],"prefix":"10.1002","volume":"8","author":[{"given":"P. T.\u2010H.","family":"Wong","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"E. G.","family":"McGeer","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"P. 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