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Excitatory amino acids are elevated in human epileptic cerebral cortex

From the Department of Neurology and Neurosurgery (Drs. Sherwin, Robitaille, Quesney, Olivier, Villemure, Leblanc, Feindel, E. Andermann, Gotman, F. Andermann, and Ethier), Montreal Neurological Institute and Hospital, McGill University, Montreal, Quebec; and the Clarke Institute of Psychiatry (Dr. Kish), Toronto, Ontario, Canada.

We used intraoperative electrocorticography to identify and compare specimens from two groups of patients undergoing temporal lobectomy: (1) spiking cortex (12 patients)—epileptic activity recorded over much of the temporal convexity; and (2) nonspiking cortex (9 patients)—temporal convexity free of interictal spiking, epileptic activity confined to the hippocampus and/or amygdala. Comparative amino acid levels were (µmol/g protein, mean ±: SEM): glutamate—spiking 109.8 ±: 1.8, nonspiking 87.4 ±: 2.0 (p < 0.001); aspartate—spiking 15.2 ±: 0.9, nonspiking 12.2 ±: 0.5 (p < 0.05); GABA—spiking 15.0 ±: 1.0, nonspiking 13.9 ±: 1.4 (NS); taurine—spiking 14.5 ±: 0.8, nonspiking 12.2 ±: 0.8 (NS); and glycine—spiking 11.5 ±: 0.8, nonspiking 7.4 ±: 0.6 (p < 0.01). Cortical epileptic activity appears to be associated with elevated concentrations of glutamate, aspartate, and glycine, but not GABA and taurine, perhaps indicating a relative imbalance between putative excitatory and inhibitory amino acid neurotransmitters.

Address correspondence and reprint requests to Dr. Sherwin, Montreal Neurological Institute, 3801 University Street, Montreal, Quebec H3A 2B4, Canada.

Supported by the Medical Research Council of Canada. Dr. Kish is a Career Scientist of the Ontario Ministry of Health.

Presented in part at the thirty-ninth annual meeting of the American Academy of Neurology, New York, NY, April 1987.

Received August 11, 1987. Accepted for publication in final form October 15, 1987.

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