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Journal of Pharmacology And Experimental Therapeutics, Vol. 120, Issue 3, 301-323, 1957
Copyright © 1957 by American Society for Pharmacology and Experimental Therapeutics

EFFECTS OF DIPHENYLHYDANTOIN ON SYNAPTIC TRANSMISSION IN CAT SPINAL CORD AND STELLATE GANGLION

Don W. Esplin 1, Dale G. Heaton 1, and Judith Coray 1

1 Department of Pharmacology, University of Utah College of Medicine, Salt Lake City

Diphenylhydantoin (Dilantin) has been studied for its effects on various aspects of synaptic transmission in 30 unanesthetized cats. The effects on spinal cord and stellate ganglion are qualitatively identical and will be summarized together.

Maximal isolated monosynaptic responses are reduced about 10 per cent by 30 mgm./kgm. of the drug. This dose reduces polysynaptic potentials by about 30 per cent. Dilantin does not affect either direct facilitation or inhibition in the spinal cord. The drug deepens presynaptic depression following transmission of an impulse and enhances transmission failure during repetitive stimulation. Response deficit referable to the drug is quite pronounced in the ganglion, but it is slight in both monosynaptic and polysynaptic pathways of the spinal cord.

Post-tetanic potentiation (PTP) is strikingly reduced by Dilantin. This reduction in PTP is attributable to specific suppression of the potentiating process. It is not dependent upon the parameters of tetanization, nor related to the effect of the drug on excitation or transmission during tetanization. None of the effects of Dilantin is antagonized by Metrazol or strychnine.

The doses of Dilantin employed in all experiments were in the anticonvulsant, nontoxic range for cats. The observed effects are discussed with regard to the anticonvulsant properties of the drug. It is specifically proposed that PTP, including enhancement of transmission during tetanic stimulation, is involved in spread of seizure discharge and that reduction of PTP by Dilantin is intimately related to its anticonvulsant action.

Submitted on February 8, 1957




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Copyright © 1957 by the American Society for Pharmacology and Experimental Therapeutics.