Recovery of vibrissae-dependent behavioral responses following barrelfield damage is not dependent upon the remaining somatosensory cortical tissue

Abstract

Previous work has demonstrated that damage to the primary somatosensory cortex produces substantial deficits in a vibrissal cue-dependent discrimination task which recover gradually over the course of post-injury testing. The present study was designed to evaluate the possible site(s) and mechanisms underlying behavioral recovery in this task. Wistar rats were trained under red light in a T-maze to produce ipsilateral turns depending upon the presence of a vibrissal cue. Animals were then subjected to photothrombotic infractions of either the ipsilateral medial parietal cortex, the ipsilateral primary and secondary somatosensory cortex (SI/SII), the primary and secondary somatosensory cortices of both hemispheres (bilateral SI/SII) or sham surgical procedures. Behavioral testing resumed 24 hours following surgery, and continued for a total of 60 days. The performance of animals with infarcts restricted to the medial parietal cortex did not differ from that of sham-operated controls. Animals with either unilateral or bilateral SI/SII infarcts exhibited a significant decrease in percent correct responding as compared to shams and rats in the medial parietal group. These deficits recovered to pre-infarct levels over approximately 35–40 days. This rate of recovery was slower than the recovery exhibited by animals given medial parietal infarcts which spared the primary barrelfield cortex. The results of this study suggest that neither the contralateral somatosensory cortex nor the vibrissal representation within ipsilateral SII cortex play a critical role in the recovery process. The possibility that subcortical structures underlie the deficits observed following barrelfield cortical damage is discussed.