Abstract

Summary Administration of semicarbazide to acute spinal cats resulted in a gradual and complete suppression of the dorsal root reflex and dorsal root potential. Semicarbazide also produced marked reduction in the long-latency inhibition as measured by monosynaptic testing. The time course of these effects correlated with the time course of the semicarbazide-induced depletion of GABA in the spinal cord. Semicarbazide had little or no effect on mono- and polysynaptic reflexes or postsynaptic inhibition. These results are consistent with the hypothesis that GABA is involved in the mediation of presynaptic inhibition.

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