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By Julius A. Vida (Eds.)

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Hence, an effective anticonvulsant drug should stabilize neuronal membranes, augment inhibitory processes, or suppress excitation. V. MECHANISM OF ANTICONVULSANT DRUG ACTION Hypotheses concerning the mechanism(s) of action of anticonvulsant drugs have been derived from observations of their effects in a variety ofneurophysiological systems. These systems include isolated peripheral nerve, neuromuscular junction preparations, spinal cord preparations, and repetitive electrical activity within and between various central nervous system structures induced by focal, electrical, or chemical stimuli.

Gallagher 4. Deoxybarbiturate (Primidone) Primidone was synthesized in 1949 (Bogue and Carrington, 1953) and introduced to clinical use in 1952 by Handley and Stewart. It is the 2-deoxy derivative of phénobarbital and represents another derivative with a spectrum of anticonvulsant and toxic activity different from that of phénobarbital. In animals and man, primidone is metabolized to phenylethylmalondiamide (PEMA) and phénobarbital (Gallagher and Baumel, 1972). Recent studies with 14C-labeled primidone found no evidence of polar metabolites of primidone or PEMA in urine from epileptic patients (Zavadil and Gallagher, 1976).

If the major input to the cell is inhibitory, the neuron is hyperpolarized and resistant to propagation of an action potential. An action potential is the result of the neuronal membrane becoming permeable to sodium ions, which causes a sudden rise in intracellular sodium 26 Brian B. Gallagher concentration. The increase in intracellular sodium changes the potential difference between the inside and outside of the cell from negative to positive. When sodium entry stops, active extrusion of sodium begins accompanied by membrane permeability to potassium, which moves out of the cell, resulting in repolarization.

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