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Journal of Pharmacology And Experimental Therapeutics, Vol. 154, Issue 1, 119-127, 1966
Copyright © 1966 by American Society for Pharmacology and Experimental Therapeutics


DIFFERENTIAL EFFECTS OF DEPRESSANT DRUGS ON PRESYNAPTIC INHIBITION

James T. Miyahara 1, Don W. Esplin 1, and Barbara Zablocka 1

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

Twelve depressant drugs were studied for their effects upon presynaptic inhibition in the spinal cord in unanesthetized spinal cats. Eight anesthetic agents (pentobarbital, phenobarbital, ethanol, chlorai hydrate, chloroform, diethyl ether, nitrous oxide and magnesium sulfate) all markedly enhanced presynaptic inhibition in doses that produced sedation or light anesthesia. This effect was also seen with the anticonvulsant drug trimethadione in anticonvulsant, nontoxic doses. Three other depressants had different effects upon presynaptic inhibition. Mephenesin blocked inhibition in doses that had little effect upon the unconditioned monosynaptic discharge. Procaine enhanced presynaptic inhibition in low doses and blocked this process in high doses. Carbon dioxide blocked presynaptic inhibition, and the degree of block was directly related to the degree of depression of the unconditioned monosynaptic response. The relationship existing between amplitude of the monosynaptic discharge and intensity of presynaptic inhibition was determined by varying the tempera-ture of the spinal cord. The intensity of inhibition was reduced as the monosynaptic spike was decreased. Only the effect of carbon dioxide on inhibition resembled the relationship obtained by changing spinal cord temperature.

Submitted on December 13, 1965
Accepted on April 28, 1966




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J. Nestoros
Ethanol specifically potentiates GABA-mediated neurotransmission in feline cerebral cortex
Science, August 8, 1980; 209(4457): 708 - 710.
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Copyright © 1966 by the American Society for Pharmacology and Experimental Therapeutics.