Human epileptic brain Na, K ATPase activity and phenytoin concentrations.
An abnormal flux of monovalent cations may be related to the epileptogenic process in man. One possible mechanism for deranged electrolyte metabolism in epileptic brain is an abnormality in sodium, potassium-dependent adenosine triphosphatase (Na, K ATPase). We found the activity of Na, K ATPase to be significantly less in epileptic human corfex than in nonepileptic cortex. Histological changes have been simultaneously evaluated in epileptic brain. A second membrane-bound enzyme, acetylcholinesterase (AChE), was also assayed as a marker for neuronal membranes and found not to correlate with the epileptogenicity of human brain. In addition, the concentrations of the anticonvulsant compound phenytoin have been determined in the serum and cerebral cortex of epileptic and nonepileptic patients. The ratio of phenytoin in cortex to serum concentration is significantly lower in epileptic patients than in nonepileptic controls.
D000110:Acetylcholinesterase / Q000378:metabolism; D000251:Adenosine Triphosphatases / Q000378:metabolism*; D000293:Adolescent; D000328:Adult; D001253:Astrocytes / Q000473:pathology; D001921:Brain / Q000378:metabolism*; D002648:Child; D004827:Epilepsy / Q000188:drug therapy / Q000201:enzymology / Q000378:metabolism* / Q000473:pathology; D006801:Humans; D007223:Infant; D009474:Neurons / Q000473:pathology; D010672:Phenytoin / Q000097:blood / Q000378:metabolism* / Q000627:therapeutic use; D011188:Potassium; D012964:Sodium
D010672:Phenytoin; D012964:Sodium; D000110:Acetylcholinesterase; D000251:Adenosine Triphosphatases; D011188:Potassium