Responses in the First or Second Somatosensory Cortical Area in Cats during Transient Inactivation of the Other Ipsilateral Area with Lidocaine Hydrochloride

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Abstract
Simultaneous recordings were obtained from the primary and secondary somatosensory cortical areas (SI and SII) in cats anesthetized with ketamine or pentobarbital. A total of 40 individual neurons were studied (29 in SII and 11 in SI) before, during, and following injections of microliter quantities of lidocaine hydrochloride in the other ipsilateral cortical area. Activity in the cortex injected with the local anesthetic was monitored with single-neuron, multineuron, or evoked potential responses to determine the time course of inactivation within 0.5-2 mm of the injection sites. Recording sites in both cortical locations were in the representations of the distal forelimb. Responses were elicited by transcutaneous electrical stimulation across the receptive fields with needle electrodes. Short-latency responses were synchronously activated, and, in those circumstances where single neurons were isolated in both areas, no overall differences in latency were noted. Anesthetization of either cortical area never blocked access of somatosensory information to the intact area, even when the injected cortex was completely silenced in the vicinity of the injection mass. In 15 SII neurons and 7 SI neurons, changes were seen in short-latency evoked responses to stimulation of their receptive fields or in background activity following local anesthesia of the other area through several cycles of injection and recovery. In 7 of these 15 SII cells, changes were noted in the timing and/or firing rates of the short-latency responses; changes were noted in the short-latency responses of 2 of these 7 SI cells while SII was silenced. In 11 SII and 6 SI cells, "background" activity that was recorded during the interstimulus intervals either increased (most cases) or decreased during local anesthesia of the other area. The results are discussed in reference to the hypothesis that primary sensory cortical areas feed information forward to secondary areas, and these feed back modulatory controls to the primary regions.