Papadopoulos Catherine M, Tsai Shih-Yen, Cheatwood Joseph L, Bollnow Melanie R, Kolb Bryan E, Schwab Martin E, Kartje Gwendolyn L
Research, Hines VA Hospital, Hines, IL 60141, USA.
Cereb Cortex. 2006 Apr;16(4):529-36. doi: 10.1093/cercor/bhi132. Epub 2005 Jul 20.
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.
我们的研究表明，成年大鼠局灶性缺血损伤后，用单克隆抗体（mAb）IN-1中和轴突生长抑制因子Nogo-A可导致功能恢复。此外，从对侧皮质到与观察到的功能恢复相对应的皮质下区域形成了新的轴突连接。本研究调查了同样有助于功能恢复的树突变化是否与缺血损伤和用mAb IN-1治疗后显示的轴突可塑性平行。检查了对侧感觉运动皮质中经高尔基-考克斯染色的V层锥体神经元，以寻找树突萌发的证据。结果表明，在有损伤的mAb IN-1治疗动物中，树突分支和棘密度增加。有趣的是，在无损伤的情况下给予mAb IN-1会导致树突短暂生长，而棘密度没有变化。这些结果表明Nogo-A在限制中风后树突可塑性方面具有新的作用。
