Abstract
Blood-spinal cord barrier (BSCB) strictly maintains the fluid microenvironment of the spinal cord within a narrow limit4,6. Alteration of the BSCB in several diseases inflicting the cord is usually associated with marked neuronal, glial and myelin cell damage21. However, the functional significance of the BSCB breakdown in inducing cell changes in the cord is still speculative. Thus, it is still not certain whether cellular changes seen in several diseases in the cord are the cause or effect of BSCB dysfunction. There are reasons to believe that breakdown of the BSCB plays important role in the cell injury caused by several noxious insults to the cord18,20. This is evident from the fact that in healthy spinal cord the BSCB is very tight to several tracers such as colloidal lanthanum (molecular diameter, MD less than 20 Å); microperoxidase (MD 20 Å), horseradish peroxidase (MD 50 Å) and ferritin (MD 100 Å)2,4,6,9,20. Previous studies from our laboratory using hydrated lanthanum (MD 9.2 Å) show that the passage of the tracer is severely restricted at the tight junctions of the spinal cord endothelial cells8,16. Furthermore, presence of lanthanum in vesicular profiles or within the endothelial cell cytoplasm is mainly absent16. This indicates that the permeability properties of the BSCB are quite similar to that of the blood-brain barrier (BBB).
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Sharma, H.S., Ove-Sjöquist, P., Westman, J. (2001). Pathophysiology of the Blood-Spinal Cord Barrier in Spinal Cord Injury. In: Kobiler, D., Lustig, S., Shapira, S. (eds) Blood—Brain Barrier. Springer, Boston, MA. https://doi.org/10.1007/978-1-4615-0579-2_32
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DOI: https://doi.org/10.1007/978-1-4615-0579-2_32
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