Effects of intravenously injected Idocaine (5 to 25 mg/kg) on synaptic transmission were studied in decerebrate or spinal cats by stimulating a dorsal lumbar root and recording the reflex action potential evoked in the ventral root. Lidocaine increased the amplitude of the monosynaptic spike two- to 25-fold, and reduced the polysynaptic response by 10 to 50 per cent of the control value. Facilitation of synaptic transmission presumably resulted from selective depression of segmental inhibitory synaptic influences and appeared unrelated to blood pressure. The convulsant action of Idocaine thus may be due to preferential depression of inhibitory control normally exerted over excitatory input