Functional recovery and neuroanatomical plasticity following middle cerebral artery occlusion and IN-1 antibody treatment in the adult rat

被引:209
作者
Papadopoulos, CM
Tsai, SY
Alsbiei, T
O'Brien, TE
Schwab, ME
Kartje, GL
机构
[1] Loyola Univ, Med Ctr, Dept Cell Biol Neurobiol & Anat, Maywood, IL 60153 USA
[2] Loyola Univ, Med Ctr, Dept Neurol, Maywood, IL 60153 USA
[3] Loyola Univ, Med Ctr, Neurosci Program, Maywood, IL 60153 USA
[4] Hines Vet Affairs Hosp, Neurol Serv, Hines, IL USA
[5] Hines Vet Affairs Hosp, Res Serv, Hines, IL USA
[6] Swiss Fed Inst Technol, Dept Biol, Zurich, Switzerland
[7] Univ Zurich, Brain Res Inst, Zurich, Switzerland
[8] Loyola Univ, Dept Math & Stat, Ctr Stat Consulting, Chicago, IL 60611 USA
[9] Swiss Fed Inst Technol, Dept Biol, Zurich, Switzerland
[10] Univ Zurich, Brain Res Inst, Zurich, Switzerland
关键词
D O I
10.1002/ana.10144
中图分类号
R74 [神经病学与精神病学];
学科分类号
摘要
Stroke is a prevalent and devastating disorder, and no treatment is currently available to restore lost neuronal function after stroke occurs. One unique therapy that may improve functional recovery after stroke is blockade of the neurite inhibitory protein Nogo-A with the monoclonal antibody IN-1, through enhancement of neuroanatomical plasticity from uninjured areas of the central nervous system. In the present study, we combined IN-1 treatment with an ischemic lesion (permanent middle cerebral artery occlusion) to determine the effect of Nogo-A neutralization on cortical plasticity and functional recovery. We report here that, following ischemic stroke and treatment with IN-1, adult rats demonstrated functional recovery on a forelimb-reaching task and new cortico-efferent projections from the opposite, unlesioned hemisphere. These results support the efficacy of Nogo-A blockade as a treatment for ischemic stroke and implicate plasticity from the unlesioned hemisphere as a mechanism for recovery.
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页码:433 / 441
页数:9
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