Cerebral Cortex Advance Access originally published online on July 20, 2005
Cerebral Cortex 2006 16(4):529-536; doi:10.1093/cercor/bhi132
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Published by Oxford University Press 2005.
Dendritic Plasticity in the Adult Rat Following Middle Cerebral Artery Occlusion and Nogo-A Neutralization
1 Research, Hines VA Hospital, Hines, IL 60141, USA, 2 Neurology Service, Hines VA Hospital, Hines, IL 60141, USA, 3 Department of Neurology, Loyola University, Maywood, IL 60153, USA, 4 Department of Psychology, University of Lethbridge, Lethbridge, AB, Canada, 5 Brain Research Institute, University of Zurich and Swiss Federal Institute of Technology, Zurich, Switzerland and 6 Department of Cell Biology, Neurobiology and Anatomy, Loyola University, Maywood, IL 60153, USA
Address correspondence to Catherine Papadopoulos, Edward Hines VA Hospital, Research Service 151, Hines, IL 60141, USA. Email: papadop{at}uic.edu.
Our work has shown that following focal ischemic lesion in adult rats, neutralization of the axon growth inhibitor Nogo-A with the monoclonal antibody (mAb) IN-1 results in functional recovery. Furthermore, new axonal connections were formed from the contralesional cortex to subcortical areas corresponding to the observed functional recovery. The present study investigated whether dendritic changes, also known to subserve functional recovery, paralleled the axonal plasticity shown after ischemic lesion and treatment with mAb IN-1. Golgi–Cox-stained layer V pyramidal neurons in the contralesional sensorimotor cortex were examined for evidence of dendritic sprouting. Results demonstrated increased dendritic arborization and spine density in the mAb IN-1-treated animals with lesion. Interestingly, administration of mAb IN-1 without lesion resulted in transient dendritic outgrowth with no change in spine density. These results suggest a novel role for Nogo-A in limiting dendritic plasticity after stroke.
Key Words: dendritic arbors and spines • Golgi–Cox • layer V • motor cortex • rat • stroke
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