Abstract
Chronic undercutting of cerebral cortex in the cat for survival periods of 9 to 308 days was found to cause an increase in duration of epileptiform electrical, afterdischarge and a significant decrease in content of glutamic acid, GABA, and aspartic acid as compared with homologous cortex of opposite hemisphere. These changes were comparable (though less marked) with changes previously found in cobalt-induced experimental epileptogenic lesions. Rate of release of GABA, glutamic acid, and aspartic acid into superfusates of undercut cortex at rest was higher in undercut cortex and was increased further by electrical stimulation. It was concluded that chronic partial denervation of cerebral cortex causes prolonged changes in metabolism or storage of glutamic acid, GABA, and aspartic acid probably related to increased tendency to prolonged epileptiform discharge similar in some respects (though not all) to changes observed in cobalt-induced cortical epileptogenic lesions. However, electrical afterdischarge threshold was not reduced in chronically undercut cortex and prolonged afterdischarge was not necessarily related to concentration of GABA in superfusate from undercut cortex, suggesting that factors other than amino acid metabolism may be also involved in mechanisms of epileptogenesis in undercut cortex.