Cortical involvement in the induction, but not expression, of thalamic plasticity.

The present study examined the role of the somatosensory cortex in the plasticity of thalamic sensory maps. Thalamic plasticity was induced by the disruption of hindlimb input by unilateral destruction of nucleus gracilis. Unilateral somatosensory cortex lesions were performed either on the same day as or a week after the removal of hindlimb input. Multiple electrode penetrations enabled us to measure the volume of somatosensory thalamus devoted to hindlimb, forepaw, and shoulder body regions. Cortical lesions alone did not change the volume of the shoulder, forepaw, or hindlimb representations in the thalamus relative to controls. However, these lesions blocked the increase in shoulder representation resulting from the nucleus gracilis lesion. In contrast, if thalamic reorganization caused by removal of hindlimb input was allowed to occur, subsequent somatosensory cortex lesions 1 week later did not prevent reorganization. Thus, an intact somatosensory cortex is necessary for the occurrence of sensory map reorganization at the thalamic level (induction) in response to nucleus gracilis lesions, but not for the maintenance of such changes once they are present (expression).