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Unilateral striatal lesions in the cat disrupt well-learned motor plans in a GO/NO-GO reaching task

dc.contributor.authorAldridge, J. Wayneen_US
dc.contributor.authorGilman, Siden_US
dc.contributor.authorThompson, J. F.en_US
dc.date.accessioned2006-09-08T19:52:22Z
dc.date.available2006-09-08T19:52:22Z
dc.date.issued1997-03en_US
dc.identifier.citationAldridge, J. W.; Thompson, J. F.; Gilman, Sid; (1997). "Unilateral striatal lesions in the cat disrupt well-learned motor plans in a GO/NO-GO reaching task." Experimental Brain Research 113(3): 379-393. <http://hdl.handle.net/2027.42/42008>en_US
dc.identifier.issn0014-4819en_US
dc.identifier.urihttps://hdl.handle.net/2027.42/42008
dc.identifier.urihttp://www.ncbi.nlm.nih.gov/sites/entrez?cmd=retrieve&db=pubmed&list_uids=9108206&dopt=citationen_US
dc.description.abstract We examined the changes in learned and spontaneous motor behavior after a unilateral excitotoxin lesion of the neostriatum. Cats were trained to perform a sensory-cued GO/NO-GO reaching task. Success rate, reaction time, movement speed and kinematic patterns were used to characterize motor system properties. In addition, motor properties before and after the lesion were compared by clinical neurological examinations and video tape observations of free-range behavior. We found that in normal animals motor performance in the task was fluent, highly automatic and skillful with consistent patterns from trial to trial and day to day. The striatal lesion resulted in a marked impairment in the animals’ ability to perform the automatic response to the sensory cues in the motor task. In contrast, sensorimotor behavior in contexts apart from the task was altered minimally, with changes that were often difficult to detect. The animals recovered their ability to perform the task gradually, although they never reached prelesion performance levels in up to 24 weeks of evaluation. The animals had difficulty making reaching movements in GO trials and, in NO-GO trials failures to withhold movements were more frequent. Failures were due to a specific inability to execute previously well-learned movements in response to cues and not to an inability to recognize and interpret the cues. The lesion effects were restricted to the automatic motor response to the learned cues, as the animals could make reaching movements to the target without obvious impairment in response to novel stimuli. They also made similar spontaneous movements apart from the motor task that appeared to be unimpaired. The unique motor style and strategies that characterized the behavior of individual animals prior to the lesion were still evident after the lesion, even though they were superimposed on lower success rates and slower movement speeds. Our findings suggest that the basal ganglia facilitate the fluent and rapid execution of sequences of well-learned sensorimotor behavior, but the representations of motor plans are not stored in the basal ganglia.en_US
dc.format.extent1249503 bytes
dc.format.extent3115 bytes
dc.format.mimetypeapplication/pdf
dc.format.mimetypetext/plain
dc.language.isoen_US
dc.publisherSpringer-Verlag; Springer-Verlag Berlin Heidelbergen_US
dc.subject.otherLegacyen_US
dc.subject.otherSensory Cuesen_US
dc.subject.otherKey Words Movementen_US
dc.subject.otherReaction Timeen_US
dc.subject.otherStriatumen_US
dc.subject.otherBasal Gangliaen_US
dc.titleUnilateral striatal lesions in the cat disrupt well-learned motor plans in a GO/NO-GO reaching tasken_US
dc.typeArticleen_US
dc.subject.hlbsecondlevelPublic Healthen_US
dc.subject.hlbsecondlevelPsychologyen_US
dc.subject.hlbsecondlevelNeurosciencesen_US
dc.subject.hlbsecondlevelMolecular, Cellular and Developmental Biologyen_US
dc.subject.hlbtoplevelSocial Sciencesen_US
dc.subject.hlbtoplevelScienceen_US
dc.subject.hlbtoplevelHealth Sciencesen_US
dc.description.peerreviewedPeer Revieweden_US
dc.contributor.affiliationumDepartment of Neurology, University of Michigan, 1103 East Huron, Ann Arbor, MI 48104-1687, USA; Tel: + 1 (313)-763-3706, Fax: +1 (313)-764-2189, e-mail: wayne.aldridge@umich.edu, US,en_US
dc.contributor.affiliationumDepartment of Neurology, University of Michigan, 1103 East Huron, Ann Arbor, MI 48104-1687, USA; Tel: + 1 (313)-763-3706, Fax: +1 (313)-764-2189, e-mail: wayne.aldridge@umich.edu, US,en_US
dc.contributor.affiliationumDepartment of Neurology, University of Michigan, 1103 East Huron, Ann Arbor, MI 48104-1687, USA; Tel: + 1 (313)-763-3706, Fax: +1 (313)-764-2189, e-mail: wayne.aldridge@umich.edu, US,en_US
dc.contributor.affiliationumcampusAnn Arboren_US
dc.identifier.pmid9108206en_US
dc.description.bitstreamurlhttp://deepblue.lib.umich.edu/bitstream/2027.42/42008/1/221-113-3-379_71130379.pdfen_US
dc.identifier.doihttp://dx.doi.org/10.1007/PL00005592en_US
dc.identifier.sourceExperimental Brain Researchen_US
dc.owningcollnameInterdisciplinary and Peer-Reviewed


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