July 30, 2007 Acute spinal cord injury can damage spinal cord tissue and result in loss of functions such as mobility or feeling.
In a study appearing online on July 26 in advance of publication in the August print issue of the Journal of Clinical Investigation, J. Marc Simard and colleagues from the University of Maryland at Baltimore show that calcium-activated cation channels in capillaries surrounding spinal cord tissue are critical to the process that causes spinal cord tissue loss after acute cord injury, and as such are a potential target in the therapy of spinal cord injuries.
The authors showed that spinal cord injury in otherwise healthy rats caused a lesion in spinal cord tissue that progressively expanded in size and was accompanied by a fragmentation of surrounding capillaries, resulting in hemorrhage, tissue necrosis, and neurological dysfunction. The expression of sulfonylurea receptor 1 (SUR1) was increased in the capillaries and neurons surrounding the lesion and also associated with expression of SUR1-regulated, calcium-activated cation channels known as NC[Ca-ATP] channels.
The authors went on to show that suppression or blockade of SUR1 activity following spinal cord injury essentially eliminated capillary fragmentation and hemorrhage, reduced spinal cord tissue damage 3-fold, and resulted in marked improvement in mobility in treated versus untreated animals.
The results of the study suggest that SUR1-regulated NC[Ca-ATP] channels in the lining of capillaries are critical to the development of progressive hemorrhagic necrosis following spinal cord injury, and as such may constitute a target for therapy in spinal cord injury.
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