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This work aimed to study the responses of cuneothalamic and thalamocortical cells to electrical stimulation of the body surface in alpha-chloralose-anaesthetized cats. It was found that both classes of cells had a central excitatory receptive field, an edge overlapping the field centre whose stimulation elicited inhibitory-excitatory (cuneothalamic cells) and excitatory-inhibitory (thalamocortical cells) sequences, and a surrounding or peripheral area usually being inhibitory. Manipulating the descending corticofugal activity by removing the fronto-parietal cortex, electrical stimulation, or by placing picrotoxin or muscimol over the sensorimotor cortex demonstrated that the cortical feedback potentiated effects driven from the field centre and the surround. In particular this potentiated centre-driven excitation and surround-driven inhibition, but some of the data points to more complex patterns. The inhibition elicited in cuneothalamic cells from the edge and the surround of the field was faster than the excitation induced from the field centre. Effects at the edge of the field centre included late excitatory responses relayed via the cerebral cortex. There were also direct corticofugal excitatory inputs to the field centre. Excitatory surrounds were occasionally observed, the assumption being that in most cases these were suppressed by the enhanced inhibition driven from the cortex. The data indicate that the cortico-subcortical feedback contributes not only to enhance the surround antagonism of a centre response but also to increase the time resolution of thalamic and cuneate relay somesthetic neurons.

The ascending cutaneous transmission through the middle cuneate nucleus is subject to cortico-feedback modulation. This work studied the intracuneate cellular mechanisms underlying the corticocuneate influence. Single unit extracellular records combined with iontophoresis showed that the corticocuneate input activates cuneo-lemniscal (CL) and noncuneo-lemniscal (nCL) cells via N-methyl-D-aspartate (NMDA) and non-NMDA receptors as shown by the decrease of the cortical-induced activation on ejection of CNQX and APV, either alone or in combination. These results were confirmed by in vivo intracellular recordings. Two subgroups of nCL cells were distinguished according to their sensitivity to iontophoretic ejection of glycine and its antagonist, strychnine. Finally, the corticalevoked activation of CL cells was decreased by GABA and increased by glycine acting at a strychnine-sensitive site, indicating that glycine indirectly affects the cuneo-lemniscal transmission. A model is proposed whereby the cortex influences CL cells through three different mechanisms, producing 1) activation via non-NMDA and NMDA receptors, 2) inhibition through GABAergic nCLs, and 3) disinhibition via serial glycinergic-GABAergic nCL cells. These corticocuneate feedback effects serve to potentiate the activity of CL cells topographically aligned through direct activation and disinhibition, while inhibiting, via GABAergic cells, other CL neurons not topographically aligned.

Intracellular recordings were obtained from cuneate neurons of chloralose-anesthetized, paralysed cats to study the synaptic responses induced by electrical stimulation of the contralateral medial lemniscus. From a total of 178 cells sampled, 109 were antidromically fired from the medial lemniscus, 82 of which showed spontaneous bursting activity. In contrast, the great majority (58/69) of the non-lemniscal neurons presented spontaneous single spike activity. Medial lemniscus stimulation induced recurrent excitation and inhibition on cuneolemniscal and non-lemniscal cells. Some non-lemniscal neurons were activated by somatosensory cortex and inhibited by motor cortex stimulation. Some other non-lemniscal cells that did not respond to medial lemniscus stimulation in control conditions were transcortically affected by stimulating the medial lemniscus after inducing paroxysmal activity in the sensorimotor cortex. These findings indicate that different sites in the sensorimotor cortex can differentially influence the sensory transmission through the cuneate, and that the distinct available corticocuneate routes are selected within the cerebral cortex. From a total of 92 cells tested, the initial effect induced by low-frequency stimulation of the sensorimotor cortex was inhibition on most of the cuneolemniscal neurons (32/52) and excitation on the majority of the non-lemniscal cells (25/40). The fact that a substantial proportion of cuneolemniscal and non-lemniscal cells was excited and inhibited, respectively, suggests that the cerebral cortex may potentiate certain inputs by exciting and disinhibiting selected groups of cuneolemniscal cells. Finally, evidence is presented demonstrating that the tendency of the cuneolemniscal neurons to fire in high-frequency spike bursts is due to different mechanisms, including excitatory synaptic potentials, recurrent activation through lemniscal axonal collaterals, and via the lemnisco-thalamo-cortico-cuneate loop.A corticocuneate network circuit to explain the results is proposed.