Dendritic Plasticity in the Adult Rat Following Middle Cerebral Artery Occlusion and Nogo-A Neutralization

• Published in: Cerebral cortex (New York, N.Y. 1991) Vol. 16; no. 4; pp. 529 - 536
• Main Authors: Papadopoulos, Catherine M., Tsai, Shih-Yen, Cheatwood, Joseph L., Bollnow, Melanie R., Kolb, Bryan E., Schwab, Martin E., Kartje, Gwendolyn L.
• Format: Journal Article
• Language: English
• Published: United States Oxford University Press 01.04.2006; Oxford Publishing Limited (England)
• Subjects: Animals; Axons - metabolism; Axons - pathology; Cerebral Cortex - metabolism; Cerebral Cortex - pathology; Dendrites - metabolism; Dendrites - pathology; dendritic arbors and spines; Golgi–Cox; layer V; Male; Middle Cerebral Artery - surgery; motor cortex; Myelin Proteins - metabolism; Nerve Regeneration - physiology; Neuronal Plasticity; Nogo Proteins; rat; Rats; Rats, Long-Evans; stroke; Stroke - metabolism; Stroke - pathology; Tissue Distribution
• ISSN: 1047-3211; 1460-2199
• DOI: 10.1093/cercor/bhi132

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.