Objective To observe the difference between blood brain barrier and blood optic nerve barrier. Methods Twenty normal male SD rat sprime; optic nerve including prelaminar region, lamina cribrosa, retro-laminar region, intraorbital portion, intracanalicular portion, and intracranial portion respectively,and cerebral cortex were removed separately. Ultrastructure of endothelial cells was observed by electron microscopy. Immunohistochemical staining was used to detect the expression of transferrin receptor (OX-26) and metalloproteinase inducer (OX-47) and extravasation of fibrinogen around microvessels. Results The results of electron microscopy showed that endothelial cells of microvessels in each portion of optic nerves and cerebral cortex did share the same tight junctions. However, the number of plasmalemmal vesicles in prelaminar region was significantly more than that in cerebral cortex(P＜0.05);there was no significant difference between other parts of optic nerves (lamina cribrosa, retro- laminar region, intraorbital portion, intracanalicular portion, and intracranial portion)and cerebral cortex in the number of the plasmalemmal vesicles(Pgt;0.05). By immunohistochemical staining，the endothelial cells of microvessels in the prelaminar region showed no expression of the OX-26 and OX-47,but extravasation of fibrinogen around microvessels was found; b positive expression of OX-26 and OX-47 was observed in the endothelial cells of the microvessels in other parts of optic nerves (lamina cribrosa, retro-laminar region, intraorbital portion, intracanalicular portion, and intracranial portion) andcerebral cortex, and no fibrinogen was seen aro und the microvessels. Conclusions There is a significant difference between the endothelial cells of the microvessels in prelaminar region and cerebral cortex in the ultrastructure, markers expression, and permeability, so the microvessel s in prelaminar region lacks the typical blood brain barrier characteristics.The microvessels in other parts of optic nerves (lamina cribrosa, retro-laminar region, intraorbital portion, intracanalicular portion, and intracranial portion) have blood brain barrier properties due to its similar specialties as which in cerebral cortex. (Chin J Ocul Fundus Dis, 2006, 22: 390-393)
Neuromyelitis spectrum disease (NMOSD) is an immune-mediated inflammatory demyelinating disease of the central nervous system. The breakdown of the blood-brain barrier (BBB), as an important link in the pathogenesis of NMOSD, has an important impact on the occurrence, development and prognosis of the disease. It is generally believed that the aquaporin 4 antibody produced in the peripheral circulation crosses the BBB cause damage to the central nervous system, and there are components involved in the destruction of BBB in the occurrence and development of NMOSD disease. At present, little is known about the molecular mechanism of BBB destruction in NMOSD lesions and there is still a lack of systematic theory. Further research and exploration of the regulatory mechanism of BBB permeability and the manifestation of barrier destruction in NMOSD diseases are of great significance for understanding the pathogenesis of NMOSD, so as to achieve early diagnosis and discover new therapeutic and preventive targets.