PARALLEL-PROCESSING OF TACTILE INFORMATION IN CAT CEREBRAL-CORTEX - EFFECT OF REVERSIBLE INACTIVATION OF SII ON SI RESPONSES

1. Responsiveness of neurons in the distal forelimb region of primary somatosensory cortex (SI) was examined in cat in association with the cooling-induced, reversible inactivation of the corresponding region o f the second somatosensory area (SII). The aim was to test whether a c omponent of the stimulus-generated tactile input to SI came via an ind irect, intracortical path from the thalamus through SIT, or whether, w hen SI responsiveness fell in association with STI inactivation, the e ffect could be explained by a disfacilitation of the SI neuron; that i s, a removal of a tonic facilitatory influence on the SI neuron that a rises from within SII. 2. The responses of 33 SI neurons to controlled tactile stimuli, usually l-s long trains of vibration or rectangular pulses delivered to the skin of the distal forelimb, were examined qua ntitatively before, during, and after the rapid, reversible inactivati on of the SII area. 3. Nineteen of the 33 neurons (similar to 60%) wer e unaffected in their response level by SII inactivation. These includ ed neurons of several functional classes whose input came from differe nt classes of tactile afferent fibers, including the Pacinian corpuscl e (PC) associated fibers, other rapidly adapting (RA) afferents from g labrous skin, and presumed hair follicle afferent (HFA) fibers. The re maining 14 neurons (similar to 40%). which also included different fun ctional classes, displayed a reduction in response level with SII inac tivation. Because this was not accompanied by significant prolongation of the SI spike waveforms, it is not attributable to direct spread of cooling from SII to SI. Construction of stimulus-response relations d emonstrated that any effect of SII inactivation on individual SI neuro ns was consistent over the whole response range. 4. The fall in respon siveness for some SI neurons in association with SII inactivation may be attributable to disfacilitation, that is, a loss of tonic facilitat ion arising in SII, rather than to a block of peripherally generated i nputs that traverse an indirect path from the skin to SI, via SII. The re are three reasons for suggesting this. First, in the course of SII cooling, the latency and time course of SI evoked potentials were not delayed in a way that might be expected if part of the SI response had come via SII. Second, the SII inactivation could reduce the SI sponta neous activity (as well as the stimulus-related responsiveness). The f acilitation from Sn is therefore not necessarily dependent on overt ta ctile stimulation, and its source may therefore be endogenous to SII. 5. Third, phase locking in the responses of SI neurons activated by vi brotactile stimuli was unchanged with SII inactivation, whether the re sponse level was reduced or unaffected. Had the tactile inputs to SI c ome via both a direct and an indirect path (through SII) from the thal amus, the inactivation of SII should have eliminated some temporal dif ferences in the inputs to the SI neurons and should have resulted in a tightening of phase locking in the responses to vibration. However, t his was not seen. 6. The results demonstrate that tactile inputs to SI are conveyed over a direct path from the thalamus and do not appear t o be carried over an indirect serially organized path through SII. How ever, there is evidence that SII can exert a background facilitatory i nfluence on SI responsiveness. The observations are qualitatively the same and quantitatively very similar to earlier ones on the effects of SI on SII responsiveness in the cat, and they confirm that, in this s pecies, SI and SIT constitute spatially separate cortical areas organi zed in parallel for the processing of incoming tactile information fro m the thalamus, but with each capable of modulatory influences on the responsiveness of the other area.