Tremor-related activity of neurons in the 'motor' thalamus: changes in firing rate and pattern in the MPTP vervet model of parkinsonism.
The pathophysiology of parkinsonian tremor remains a matter of debate with two opposing hypotheses proposing a peripheral and a central origin, respectively. A central origin of tremor could arise either from a rhythmic activity of the internal segment of the globus pallidus (GPi) or from a structure such as the thalamus, outside the basal ganglia. In this study, single-unit recordings were performed in three 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine-treated monkeys within the GPi and within three territories of the motor thalamus (delimited by their afferent inputs from the GPi, the substantia nigra and the cerebellum, respectively). For each recorded neuron, we compared the variations in firing rate and pattern in tremor and no tremor periods. Tremor either occurred spontaneously or was induced by external stimulation. When the animals entered into a tremor period we observed: (i) an increase in the mean firing rate in about half of the recorded neurons of the motor thalamus; and (ii), a change from an irregular to a rhythmic discharge within the range of tremor frequency (5-7 Hz) in about 10% of the recorded neurons of the motor thalamus (pallidal and cerebellar territories) and the GPi. Most of the thalamic neurons that exhibited a rhythmic discharge during tremor were found to be sensitive to external stimulation. Because the changes in firing rate occurred predominantly in the motor thalamus and not in the GPi, and because a fast rhythmic discharge of 10-15 Hz was frequently observed in the GPi and not in the motor thalamus, we conclude that thalamic activity is not a simple reproduction of basal ganglia output. Moreover, we suggest that thalamic processing of basal ganglia outputs could participate in the genesis of tremor, and that this thalamic processing could be influenced by sensory inputs and/or changes in attentional level elicited by external stimulation.
Guehl
D
D
INSERM U 289 Experimental Neurology and Therapeutics, Hôpital de La Salpêtrière, 47 bd de l'Hôpital, 75651 Paris cedex 13, France. ltremb@ccr.juissieu.fr
Pessiglione
M
M
François
C
C
Yelnik
J
J
Hirsch
E C
EC
Féger
J
J
Tremblay
L
L
D000200:Action Potentials / Q000502:physiology; D000818:Animals; D001479:Basal Ganglia / Q000503:physiopathology; D002531:Cerebellum / Q000503:physiopathology; D002522:Chlorocebus aethiops; D004195:Disease Models, Animal; D004576:Electromyography / Q000379:methods; D004594:Electrophysiology; D005917:Globus Pallidus / Q000503:physiopathology; D020267:MPTP Poisoning / Q000503:physiopathology*; D008297:Male; D009132:Muscles / Q000503:physiopathology; D009474:Neurons / Q000502:physiology*; D010812:Physical Stimulation; D013378:Substantia Nigra / Q000503:physiopathology; D013788:Thalamus / Q000033:anatomy & histology / Q000503:physiopathology*; D014202:Tremor / Q000209:etiology / Q000473:pathology*