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Journal of Neuroscience, Vol 15, 6531-6541, Copyright © 1995 by Society for Neuroscience
In a rat model of parkinsonism, lesions of the subthalamic nucleus reverse increases of reaction time but induce a dramatic premature responding deficit
C Baunez, A Nieoullon and M Amalric
Laboratoire de Neurobiologie Cellulaire et Fonctionnelle, CNRS, Marseille, France.
Lesions of the subthalamic nucleus (STN) have been found to reduce the
severe akinetic motor symptom produced in animal models of Parkinson's
disease, such as in monkeys treated with 1-methyl-4-phenyl-1,2,3,6-
tetrahydropyridine (MPTP) or in monoamine-depleted rats. However, little is
known about the effect of STN exclusion on subtle motor deficits induced by
moderate dopaminergic lesions in complex motor tasks. The present study was
thus performed on rats trained in a reaction time (RT) task known to be
extremely sensitive to variations of dopamine transmission in the striatum.
Animals were trained to release a lever after the onset of a visual
stimulus within a time limit to obtain a food reward. Discrete dopamine
depletion produced by infusing the neurotoxin 6-hydroxydopamine (6-OHDA)
bilaterally into the dorsal part of the striatum, produced motor initiation
deficits which were revealed by an increase in the number of delayed
responses (lever release after the time limit) and a lengthening of RTs. In
contrast, bilateral excitotoxic lesion of the STN with ibotenic acid
induced severe behavioral deficits which were opposite to those produced by
the dopaminergic lesion, as shown by an increase in the number of premature
responses (lever release before the onset of the visual stimulus) and a
decrease of RTs. Surprisingly, the performance of the animals bearing a
double lesion (striatal dopaminergic lesion followed 14 d later by STN
ibotenic lesion) was still impaired 40 d after the ibotenic lesion. As
expected, the 6-OHDA-induced motor initiation deficits were reversed by a
subsequent STN lesion. However, the dramatic increase of premature
responses contributing to major behavioral deficits induced by the STN
lesion remained unchanged. Thus, the bilateral lesion of the STN was found
to alleviate the motor deficits in this model of parkinsonism, but
essentially produced over time, long lasting deficits that might be related
to dyskinesia or cognitive impairment. The present results strongly support
the recent concept of a predominant control of the STN on basal ganglia
output structures.
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