Parallel processing of tactile information in cat cerebral cortex: effect of reversible inactivation of SII on SI...

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 of the second somatosensory area (SII). The aim was to test whether a component of the stimulus-generated tactile input to SI came via an indirect, intracortical path from the thalamus through SII, or whether, when SI responsiveness fell in association with SII inactivation, the effect could be explained by a disfacilitation of the SI neuron; that is, a removal of a tonic facilitatory influence on the SI neuron that arises from within SII. 2. The responses of 33 SI neurons to controlled tactile stimuli, usually 1-s long trains of vibration or rectangular pulses delivered to the skin of the distal forelimb, were examined quantitatively before, during, and after the rapid, reversible inactivation of the SII area. 3. Nineteen of the 33 neurons (approximately 60%) were unaffected in their response level by SII inactivation. These included neurons of several functional classes whose input came from different classes of tactile afferent fibers, including the Pacinian corpuscle (PC) associated fibers, other rapidly adapting (RA) afferents from glabrous skin, and presumed hair follicle afferent (HFA) fibers. The remaining 14 neurons (approximately 40%), which also included different functional classes, displayed a reduction in response level with SII inactivation. 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 demonstrated that any effect of SII inactivation on individual SI neurons was consistent over the whole response range. 4. The fall in responsiveness for some SI neurons in association with SII inactivation may be attributable to disfacilitation, that is, a loss of tonic facilitation arising in SII, rather than to a block of peripherally generated inputs that traverse an indirect path from the skin to SI, via SII. There 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 spontaneous activity (as well as the stimulus-related responsiveness). The facilitation from SII is therefore not necessarily dependent on overt tactile stimulation, and its source may therefore be endogenous to SII.(ABSTRACT TRUNCATED AT 400 WORDS)