Electrophysiological study of dyskinesia produced by microinjection of picrotoxin into the striatum of the rat.
The neuronal mechanism of dyskinesia of the contralateral forelimb produced by microinjection of picrotoxin (PTX), a GABA antagonist, into the caudoputaminal unit (CPU) was analyzed electrophysiologically. PTX injection resulted in production of sharp, negative field potentials with or without preceding or succeeding positivity in the CPU and cerebral cortex (CX). These spike potentials first appeared in the CPU, thereafter within the CX, and were finally accompanied by dyskinesia indicated by electromyogram activity of the forelimb in association with fully developed CX spike potentials. Dyskinesia disappeared reversibly by cooling, and irreversibly by ablation, of the CX, indicating the crucial participation of the CX in the manifestation of dyskinesia. CPU spike potentials remained even after isolation of the CPU from its major afferents. Grouped discharges of extracellularly recorded single-unit spikes were observed in the CPU in association with the development of CPU spike potentials. Single-unit spikes of the pars reticulata of the substantia nigra were inhibited, and those of the ventromedial nucleus (VM) of the thalamus were excited in association with CPU spike potentials. We therefore propose that the primary origin of the dyskinesia is the CPU and that the inhibitory CPU efferent, as well as the nigrothalamic, pathway plays a basic role in the manifestation of the dyskinesia.
Muramatsu
S
S
Department of Neurology, Jichi Medical School, Tochigiken, Japan.
Yoshida
M
M
Nakamura
S
S
D000200:Action Potentials / Q000187:drug effects; D000818:Animals; D002540:Cerebral Cortex / Q000503:physiopathology*; D003080:Cold Temperature; D003342:Corpus Striatum / Q000187:drug effects / Q000503:physiopathology*; D004409:Dyskinesia, Drug-Induced / Q000503:physiopathology*; D005260:Female; D008297:Male; D008845:Microinjections; D010852:Picrotoxin; D051381:Rats; D011919:Rats, Inbred Strains
D010852:Picrotoxin