Functional recovery and neuroanatomical plasticity following middle cerebral artery occlusion and IN-1 antibody treatment in the adult rat.
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.
Papadopoulos
Catherine M
CM
Neurology and Research Services, Hines Veterans Affairs Hospital, Hines, IL 60153, USA.
Tsai
Shih-Yen
SY
Alsbiei
Talal
T
O'Brien
Timothy E
TE
Schwab
Martin E
ME
Kartje
Gwendolyn L
GL
D000367:Age Factors; D000818:Animals; D000911:Antibodies, Monoclonal / Q000493:pharmacokinetics*; D005247:Feeding Behavior; D020244:Infarction, Middle Cerebral Artery / Q000503:physiopathology* / Q000628:therapy*; D008297:Male; D009185:Myelin Proteins / Q000276:immunology*; D009473:Neuronal Plasticity; D000070798:Nogo Proteins; D051381:Rats; D020318:Rats, Long-Evans; D020127:Recovery of Function; D013003:Somatosensory Cortex / Q000502:physiology; D020521:Stroke / Q000503:physiopathology / Q000628:therapy
D000911:Antibodies, Monoclonal; D009185:Myelin Proteins; D000070798:Nogo Proteins; C000603197:Rtn4 protein, rat