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J Neurophysiol 99: 1057-1076, 2008. First published December 12, 2007; doi:10.1152/jn.01010.2007
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Testing Basal Ganglia Motor Functions Through Reversible Inactivations in the Posterior Internal Globus Pallidus

M. Desmurget2,3 and R. S. Turner1,3

1Departments of Neurobiology and Bioengineering, Center for the Neural Basis of Cognition, University of Pittsburgh, Pittsburgh, Pennsylvania; 2Centre for Cognitive Neuroscience, Centre National de la Recherche Scientifique, Unité Mixte de Recherche 5229, Bron, France; and 3Department of Neurosurgery, University of California San Francisco, San Francisco, California

Submitted 11 September 2007; accepted in final form 11 December 2007

To test current hypotheses on the contribution of the basal ganglia (BG) to motor control, we examined the effects of muscimol-induced inactivations in the skeletomotor region of the internal globus pallidus (sGPi) on visually directed reaching. Injections were made in two monkeys trained to perform four out-and-back reaching movements in quick succession toward four randomly selected target locations. Following sGPi inactivations the following occurred. 1) Peak velocity and acceleration were decreased in nearly all sessions, whereas movement duration lengthened inconsistently. 2) Reaction times were unaffected on average, although minor changes were observed in several individual sessions. 3) Outward reaches showed a substantial hypometria that correlated closely with bradykinesia, but directional accuracy was unaffected. 4) Endpoint accuracy was preserved for the slow visually guided return movements. 5) No impairments were found in the rapid chaining of out-and-back movements, in the selection or initiation of four independent reaches in quick succession or in the quick on-line correction of initially misdirected reaches. 6) Inactivation-induced reductions in the magnitude of movement-related muscle activity (EMG) correlated with the severity of slowing and hypometria. There was no evidence for inactivation-induced alterations in the relative timing of EMG bursts, excessive cocontraction, or impaired suppression of antagonist EMG. Therefore disconnecting the BG motor pathway consistently produced bradykinesia and hypometria, but seldom affected movement initiation time, feedback-mediated guidance, the capacity to produce iterative reaches, or the ability to abruptly reverse movement direction. These results are discussed with reference to the idea that the BG motor loop may regulate energetic expenditures during movement (i.e., movement "vigor").


Address for reprint requests and other correspondence: R. S. Turner, Department of Neurobiology, University of Pittsburgh, 4074 BST-3, 3501 Fifth Ave., Pittsburgh, PA 15261 (E-mail: rturner{at}pitt.edu)




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