Please use this identifier to cite or link to this item:
Title: Spinal cord injury-induced astrocyte migration and glial scar formation: Effects of magnetic stimulation frequency
Authors: Li, Zhe
Fang, Zheng-Yu
Xiong, Liang
Huang, Xiao-Lin
Keywords: Astrocyte migration;Extracellular signal-regulated kinase1/2 pathway;Magnetic stimulation;Spinal cord injury;Glial scar formation
Issue Date: Dec-2010
Publisher: NISCAIR-CSIR, India
Abstract: The effects of magnetic stimulation on spinal cord injury-induced migration of white matter astrocytes were studied using an established animal model. Ethidium bromide was injected into the dorsal spinal cord funiculus of adult Sprague-Dawley rats on the left side at T10-11. Animals then received 1.52 Tesla-pulsed magnetic stimulation for 5 min at different frequencies (0-20 Hz) for 14 consecutive days. Selected animals received the non-competitive MEK1/2 inhibitor U0126 (10 μM), prior to stimulation at 10 Hz. Lesion volumes were measured in hematoxylin/eosin-stained sections. Expression of glial fibrillary acidic protein (GFAP), microtubule associated protein-2 (MAP-2) and extra-cellular signal-regulated kinase1/2 (ERK1/2) near the epicenter of injury was examined by Western blotting with quantification using an image analysis system. Lesion volumes decreased and GFAP and p-ERK1/2 expression increased with increasing magnetic stimulation frequency (0-10 Hz). MAP-2 expression was not affected at any frequency. Pretreatment with U0126 reduced GFAP and ERK1/2 expression and increased lesion volumes in response to stimulation at 10 Hz. It is concluded that magnetic stimulation increases the migration of astrocytes to spinal cord lesions. Activation of the ERK1/2 signaling pathway is proposed to mediate astrocyte migration and glial scar formation in response to spinal cord injury.
Page(s): 359-363
ISSN: 0975-0959 (Online); 0301-1208 (Print)
Appears in Collections:IJBB Vol.47(6) [December 2010]

Files in This Item:
File Description SizeFormat 
IJBB 47(6) 359-363.pdf198.42 kBAdobe PDFView/Open

Items in NOPR are protected by copyright, with all rights reserved, unless otherwise indicated.