期刊
MOLECULAR AND CELLULAR NEUROSCIENCE
卷 39, 期 2, 页码 152-160出版社
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.mcn.2008.06.005
关键词
Antisense oligonucleotide; Gap junctions; Rat; Compression; Transection; Astrocytes; Glial fibrillary acidic protein; Microglia; Activation; Neutrophils; Vascular endothelial cells; Vascular permeability; Behavioural testing
资金
- International Spinal Research Trust
- New Zealand Marsden Fund
After traumatic CNS injury, a cascade of secondary events expands the initial lesion. The gap-junction protein connexin43 (Cx43), which is transiently up-regulated, has been implicated in the spread of 'bystander' damage. We have used an antisense oligodeoxynucleotide (asODN) to suppress Cx43 up-regulation in two rat models of spinal cord injury. Within 24 h of compression injury, rats treated with Cx43-asODN scored higher than sense-ODN and vehicle-treated controls on behavioural tests of locomotion. Their spinal cords showed less swelling and tissue disruption, less up-regulation of astrocytic GFAP, and less extravasation of fluorescently-labelled bovine serum albumin and neutrophils. The locomotor improvement Was Sustained over at least 4 weeks. Following partial spinal cord transection, Cx43-asODN treatment reduced GFAP immunoreactivity, neutrophil recruitment, and the activity of OX42(+) microglia in and around the lesion site. Cx43 has many potential roles in the pathophysiology of CNS injury and may be a valuable target for therapeutic intervention. (c) 2008 Elsevier Inc. All rights reserved.
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