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The Journal of Neuroscience, June 15, 2003, 23(12):4826-4830

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Functional Reorganization of the Motor Cortex in Adult Rats after Cortical Lesion and Treatment with Monoclonal Antibody IN-1

April J. Emerick,^1,2 Edward J. Neafsey,^2,4 Martin E. Schwab,^5,6 and Gwendolyn L. Kartje^1,2,3,4

¹Research and Neurology Service, Edward Hines Veterans Affairs Hospital, Hines, Illinois 60141 ²Neuroscience Program and Departments of ³ Neurology and ⁴Cell Biology, Neurobiology, and Anatomy, Loyola University Medical Center, Maywood, Illinois 60153, and ⁵Brain Research Institute, University of Zurich, and ⁶Department of Biology, Swiss Federal Institute of Technology, Zurich, CH-8057 Switzerland

We previously reported anatomical plasticity in the adult motor cortex after a unilateral sensorimotor cortex (SMC) lesion and treatment with monoclonal antibody (mAb) IN-1, which permits neurite outgrowth from the intact, opposite cortex into deafferented subcortical targets. This study was designed to investigate whether treatment with the mAb IN-1 after SMC lesion in the adult leads to functional reorganization of the intact, opposite motor cortex. Adult rats underwent unilateral SMC aspiration lesion and treatment with either mAb IN-1 or control antibody, or no treatment. After a 6 week survival period, the intact, opposite forelimb motor cortex was explored using intracortical microstimulation to evoke forelimb movements. A dramatic increase in ipsilateral movements of the lesion-impaired forelimb was found in animals treated with mAb IN-1 compared with control animals. These results resembled our previous findings of cortical reorganization in the spared hemisphere after neonatal cortical lesion and without any additional treatment. These results show that, after adult cortical lesion, treatment with mAb IN-1 induces a functional reorganization of the intact, opposite motor cortex.

Key words: motor cortex; intracortical microstimulation; Nogo-A; corticospinal tract; cortical injury; plasticity

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Received Dec. 5, 2002; revised Apr. 17, 2003; accepted Apr. 23, 2003.

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