Stimulation of internal capsule, thalamic sensory nucleus (VPM) and cerebral cortex inhibited deafferentation hyperactivity provoked after gasserian ganglionectomy in cat.

Facilitation of the opiate-mediated system provides relief of excess pain but not of deafferentation pain. Influence on neuronal hyper-activity, which was provoked after the deafferentation of the peripheral trigeminal nerve (deafferentation hyperactivity; DH), by stimulation of the internal capsule (IC), VPM nucleus of the thalamus and by the cerebral sensorimotor cortex, was examined. This experiment demonstrates that a suppressive effect is exerted on the sustained neuronal hyperactivity, which was proved to have a close relationship with deafferentation pain. In the preliminary experiment, it was confirmed that DH was provoked by coagulation of unilateral (left side) Gasserian ganglion in 29 adult cats, who were allowed to survive up to 72 days. DH, sustained high amplitude discharge without any stimuli on the face or neck, was detected in the subnucleus caudalis of the spinal trigeminal nucleus (STNcd) of the denervated side. DH was never suppressed by facilitation of the opiate-mediated system. 87 of 113 neurones identified in the STNcd of the denervated side showed DH in another 18 cats. In 30 of 55 neurones examined, DH was conspicuously suppressed by the stimulation of contralateral (right) side, 11 of 29 neurones by ipsilateral IC. Five of 13 neurones were suppressed by contralateral VPM stimulation, 2 of 3 neurones by ipsilateral stimulation. Stimulation of cortical area, SM1 of MS1, in other 15 cats, considerably suppressed DH in STNcd. Microinjection of wheat-germ-agglutinin in the cerebral cortex revealed in direct projection of the descending fibre from MS1 to STNcd and brain stem reticular formation via IC.(ABSTRACT TRUNCATED AT 250 WORDS)