Alterations in intralaminar and motor thalamic physiology following nigrostriatal dopamine depletion.

The response of central median/central lateral (CM/CL) and ventral anterior/ventral lateral (VA/VL) thalamic neurons to tactile sensory stimulation of the face and electrical stimulation of the striatum was assessed in awake cats before and after 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) exposure. When cats exhibited Parkinson-like motor deficits, there was a significant decrease in the number of CM/CL and VA/VL neurons responsive to tactile stimulation of the face. Mean spontaneous firing rates decreased by 58% in the CM/CL nuclei, 65% in the VA, and 49% in the VL. The number of thalamic neurons responding to electrical stimulation of the striatum was also significantly decreased in parkinsonian animals. Approximately 6 weeks after MPTP exposure, when cats had spontaneously recovered gross motor function, thalamic responses to peripheral sensory stimulation, electrical stimulation of the CD, and spontaneous activity rates, returned to approximately normal levels in all thalamic areas studied. These findings support the concept that abnormalities in the transmission of information through the thalamus, and in particular, a decrease in sensory responsiveness in intralaminar and motor thalamic regions subsequent to nigrostriatal dopamine depletion, may contribute to the generation of Parkinson-like motor and sensorimotor deficits.