The effects of lidocaine on optic evoked potentials (OEP) of the cat's visual cortex in response to electrical stimulation of the optic nerve in light and in darkness were investigated. EEC, ECG, and blood pressure were recorded simultaneously in barbiturate-anesthetized as well as in immobilized cats. In light, less than 1 mg/kg had no effect in anesthetized cats, but 1 mg/kg facilitated OEP, whereas in darkness, with OEP at naturally lower levels, both 0.5 and 1 mg/kg facilitated OEP, and the magnitude of facilitation was greater than that in light. In light, as much as 8 mg/kg was necessary for facilitation of OEP in immobilized cats, but twice that dose had no detectable effect. In darkness, with OEP naturally lower, 8 mg/kg lidocaine not only facilitated OEP in immobilized cats, but the magnitude of facilitation was greater than that in light, and 16 nig/kg also facilitated OEP. In darkness, the difference between 8 and 16 mg/kg was that with the latter dose facilitation was more predictable and longer-lasting. Facilitation of OEP by lidocaine was unrelated to its effects on blood pressure, ECG, or EEG. It is suggested that lidocaine-induced convulsions arc due to a dissociation in neuronal integration that results from depression of the active inhibitory inputs of the neuronal circuitry, that darkness induced depression of OEP is an active inhibition and that barbiturate anesthetization spares quantitatively greater inhibitory processes and thereby alters the process of homeostasis.