Interactions between somatosensory afferents arriving from different points in the periphery play an important role in sensory discrimination and also provide the substrate for plasticity following peripheral injury. To examine the extent and time course of such interactions, extracellular recordings were made from neurons in the primary somatosensory cortex and the ventroposterior lateral thalamus of anesthetized raccoons. Interactions between adjacent digits were studied using the conditioning-test paradigm in which a test pulse was delivered to the digit containing the neuron's receptive field (the on-focus digit) at various intervals following conditioning stimulation of an adjacent, off-focus digit. Off-focus stimulation produced predominantly inhibition of the test response with a maximum effect at 20-40 ms in both cortex and thalamus. The mean inhibition was approximately twice as large in the thalamus as in the cortex. Recordings were made in other animals after unmyelinated C fibers had been destroyed in the on-focus digit by subcutaneous injection of capsaicin. This resulted in a doubling of the responses evoked by the test stimulus in both regions, but the spontaneous discharge rate was not changed. The amount of inhibition produced in the cortex was unchanged by capsaicin treatment, but was reduced in the thalamus compared to control animals. This indicates that capsaicin-sensitive peripheral afferents provide a tonic control over interdigit inhibition in the thalamus.

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. The processing of sensory information by the CNS is complicated by the complex interconnections between subcortical and cortical areas. Connections between the thalamus and cortex are largely reciprocal (1) with information being processed in both feed-forward (periphery to thalamus to cortex) and feedback (corticothalamic) directions. Although the majority of studies have concentrated on the ascending or feed-forward system, the feedback connections are actually much more numerous than the thalamocortical axons (1) and may contribute to focusing of information processing in the visual (2), auditory (3, 4), and somatosensory thalamus (5). Recently it has been proposed that this feedback from the cortex may contribute to plasticity in the ventroposterior lateral (VPL) nucleus, the main thalamic relay in the somatosensory system (6-8).The corticothalamic axons are excitatory, glutamatergic, and reciprocally focused on the thalamic neurons that project to the same cortical region (1). In addition to exciting thalamocortical relay neurons directly, they also produce inhibition by means of local ␥-aminobutyric acid (GABA)ergic interneurons, which are present in most species but not rats (9), and GABAergic neurons of the reticular thalamic nucleus, which project back into VPL (10). Electrophysiological studies have confirmed the monosynaptic excitatory and disynaptic inhibitory responses in VPL relay cells when cortical output cells are stimulated (11). Studies on the function of this fe...