The influence of corticothalamic projections on the thalamus during different stages of reorganization was determined in anesthetized raccoons that had undergone previous removal of a single forepaw digit. Single-unit recordings were made from 522 sites in the somatosensory nucleus of the thalamus (ventroposterior lateral nucleus) before and after lesioning parts of primary somatosensory cortex. In those parts of ventroposterior lateral nucleus that had intact input from the periphery, the cortical lesion resulted in an immediate 85% increase in receptive field (RF) size. In animals studied 2–6 weeks after digit amputation, peripherally denervated thalamic neurons had unique RFs that were larger than normal, and these were not further enlarged by cortical lesion. However, at longer periods of reorganization (>4 mo), when the new RFs of denervated neurons had decreased in size, cortical lesion again produced expansion of RF size. These data demonstrate that corticothalamic fibers modulate the spatial extent of thalamic RFs in intact animals, probably by controlling intrathalamic inhibition. This corticothalamic modulation is ineffective during the early stages of injury-induced reorganization when new RFs are being formed, but is reinstated after the new RFs have become stabilized. The fact that neurons in the denervated thalamic region retained their unique RFs after cortical lesion indicates that their new inputs are not being relayed from a reorganized cortex and support the view that some plasticity occurs in or below the thalamus.
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