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1 Neurology, University of Rochester Medical Center, Rochester, New York, United States
2 Landon Center on Aging, Kansas University Medical Center, Kansas City, Kansas, United States; Mental Retardation Research Center, Kansas University Medical Center, Kansas City, Kansas, United States; Molecular and Integrative Physiology, Kansas University Medical Center, Kansas City, Kansas, United States
3 Center for Biostatistics and Advanced Informatics, Kansas University Medical Center, Kansas City, Kansas, United States; Department of Preventive Medicine and Public Health, Kansas University Medical Center, Kansas City, Kansas, United States
* To whom correspondence should be addressed. E-mail: Numa_Dancause{at}urmc.rochester.edu.
Following a cortical lesion, cortical areas distant from the site of injury are known to undergo physiological and anatomical changes. However, the mechanisms through which reorganization of distant cortical areas is initiated are poorly understood. In a previous publication we showed that the ventral premotor cortex (PMv) undergoes physiological reorganization following a lesion destroying the majority of the primary motor cortex (M1) distal forelimb representation (DFL). After large lesions destroying more than 50% of the M1 DFL, the PMv DFL invariably increased in size and the amount of the increase was positively correlated with the size of lesion. To determine whether lesions destroying less than 50% of the M1 DFL followed a similar trajectory, we documented PMv reorganization using intracortical microstimulation techniques following small, ischemic lesions targeting sub-regions within the M1 DFL. In contrast to earlier results, lesions resulted in a reduction of the PMv DFL regardless of their location. Further, since recent anatomical findings suggest a segregation of PMv connectivity with M1, we examined two lesion characteristics that may drive alterations in PMv physiological reorganization: location of the lesion with respect to PMv connectivity, and relative size of the lesion. The results suggest that after a lesion in the M1 DFL, the induction of representational plasticity PMv, as evaluated using ICMS, is related more to the size of the lesion than to the disruption of its intracortical connections.
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