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Department of Neurological Surgery, University of Washington, Seattle, WA.
We used both intracellular and field potential recordings to study the effects of phenytoin (20 to 40 µg per milliliter) on CA3 and CA1 neurons of guinea pig hippocampal slices, with or without exposure to the convulsant sodium penicillin G. Phenytoin did not change resting membrane potential, input resistance, action potential amplitude or duration, or the threshold intensity for activating action potentials or bursts with intracellular current pulses. Suppression of penicillin-induced bursting was associated with an increased threshold for orthodromically activating neurons. The intrinsic bursting mechanisms of the cells remained intact. Phenytoin seemed to suppress penicillin-induced epileptiform activity by decreasing synaptic transmission.
Address correspondence and reprint requests to Dr. Schneiderman, Room 115116, E. K. Jones Building, Wellesley Hospital. 160 Wellesley Street East, Toronto, Ontario M4Y 1J3, Canada.
Dr. Schneiderman was supported by a fellowship from the Medical Research Council of Canada. This work was supported by grants Nos. NS00413 and NS-04053 from the National Institute of Neurological and Communicative Disorders and Stroke. National Institute of Health, Dr. Schwartzkroin is an affiliate of the Child Development and Mental Retardation Center, University of Washington.
Presented at the thirty-third annual meeting of the American Academy of Neurology. Toronto. Canada, April 1981.
Accepted for publication November 10, 1981.
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