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Prior to implantation of the thalamic- or motor cortex-stimulating electrodes for relieving chronic pain, extracellular unitary activity was recorded and local microstimulation was done, by using microelectrodes, mainly in the ventral caudal nucleus of the thalamus. A significant number of high frequency discharge neurons (hyperactive neurons) were recorded and showed three types of discharge patterns with different interval histograms. In animal experiments, unilateral dorsal root sectioning from C5 to Th1 of male Wistar rats was made according to the method of Lombard et al[4]. One to three months after the operation, cellular activity was recorded from the contralateral thalamic nuclei (VP, zona incerta), lemniscus medialis and striatum. Hyperactive neurons were recorded from the thalamic nuclei and lemniscus medialis. The firing patterns and distribution of hyperactive neurons in these animals were very similar to those of humans. Hyperactive neurons were examined via electrical stimulation of and/or iontophoretical application of chemical substances. Hyperactive neurons were unaffected by electrical stimulation of the nucleus raphe dorsalis and locus ceruleus. However, sensorimotor cortical stimulation showed a reduction of firing in the hyperactive neurons. Iontophoretic application of glutamate showed increase in firing and GABA showed remarkable firing suppression. These results suggested that hyperactive neurons of the thalamic nuclei receive a facilitatory effect from the sensorimotor cortex with little influence from adrenergic or serotonergic systems, and these neurons have a relationship to the glutamatergic and GABAergic fibers or receptors.
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