Disease relevance of Blood-Nerve Barrier

• There remain however, many unresolved questions, such as how monoclonal anti-MAG IgM antibodies cross the blood-nerve barrier and trigger a chronic demyelinating polyneuropathy while the central nervous system is essentially spared [1].
• Our results suggest that nerve edema and increased blood-nerve barrier PA are secondary to polyol production and can be prevented by inhibiting aldose reductase [2].
• These findings demonstrate that TM is present in human nerve microvasculature but is regionally deficient in proximity to the blood-nerve barrier, which may predispose nerve to microvascular ischemia in inflammatory/prothrombotic conditions [3].

High impact information on Blood-Nerve Barrier

• A Drosophila neurexin is required for septate junction and blood-nerve barrier formation and function [4].
• Gliotactin, a novel transmembrane protein on peripheral glia, is required to form the blood-nerve barrier in Drosophila [5].
• In this study, we have successfully passively transferred disease using sera and purified IgG from 4 of 12 patients responsive to plasma exchange by bypassing the blood-nerve barrier by intraneural injection or opening it by activated T cells [6].
• This study demonstrates breakdown of the blood-nerve barrier by activated T cells, even of nonneural specificity, allowing the development of focal conduction block and demyelination in the presence of circulating antimyelin antibodies [7].
• Activity of MMPs could participate in the disruption of the blood-nerve barrier, breakdown of the myelin sheath, the release of TNF-alpha, and facilitate leukocyte invasion into the PNS [8].

Chemical compound and disease context of Blood-Nerve Barrier

• Prevention of nerve edema and increased blood-nerve barrier permeability-surface area product in galactosemic rats by aldose reductase or thromboxane synthetase inhibitors [2].
• It has been suggested that high-dose intrathecal lidocaine induces irreversible conduction block and even ischemia in white matter tracts by breakdown of the blood-nerve barrier [9].

Biological context of Blood-Nerve Barrier

• Here, we describe the molecular genetic analysis of gliotactin, a novel transmembrane protein that is transiently expressed on peripheral glia and that is required for the formation of the peripheral blood-nerve barrier [5].
• These results suggest that recovery of function is more rapid with daily administration of FK506 than with CsA or no treatment, perhaps because of earlier restoration of the blood-nerve barrier [10].
• The active transport of D-glucose from the vascular to the neural compartment requires the presence of a carrier molecule at the blood-brain and the blood-nerve barrier [11].
• Comparison of nerve regeneration in vascularized and conventional grafts: nerve electrophysiology, norepinephrine, prostacyclin, malondialdehyde, and the blood-nerve barrier [12].

Anatomical context of Blood-Nerve Barrier

• Other apolipoproteins (apo A1 and albumin) were not synthesized in the endoneurium, but they entered edematous nerves, presumably through an early breakdown in the blood-nerve barrier [13].
• Permeability-surface area products (PA) were determined with a quantitative in vivo injection technique at the blood-nerve barrier of tibial nerve, and at the blood-brain barrier, in control and streptozotocin-induced diabetic rats [14].
• In human lung at all ages, our studies revealed an approximately 45- to 50-kDa Glut-1 protein band in entrapped erythrocytes and perineural sheaths, which serve as a blood-nerve barrier [15].
• Hydrolase activity rose to 20% in the brains and exceeded control values in the sciatic nerves of transplanted twitcher mice, indicating entry of at least some donor-derived cells and/or hydrolase across the blood-brain and blood-nerve barriers after BU and HCT.(ABSTRACT TRUNCATED AT 250 WORDS)[16]
• The present investigation suggested that P-gp in the endothelial cells of the peripheral nerves might play a very important role as a part of the blood-nerve barrier function, since P-ag acts as an extension pump in these cells [17].

Associations of Blood-Nerve Barrier with chemical compounds

• Nerve water content and the permeability-surface area product (PA) to [3H]-or [14C]sucrose at the blood-nerve barrier were determined in unanesthetized control rats fed a normal diet and in rats fed galactose with or without an aldose reductase inhibitor (Statil or AL 1576) or a thromboxane synthetase inhibitor (CGS 12970) [2].
• In galactosemic rats, the mean PA to sucrose at the blood-nerve barrier, calculated from nerve dry weight, was twofold higher than in control rats [2].
• The mechanism of transfer of glucose across the blood-nerve barrier is unclarified [18].
• To study the blood-nerve barrier, fluorescein isothiocyanate-labelled albumin was given intravenously after intraneural injection [19].
• CONCLUSION: A breakdown in the blood-nerve barrier as observed on gadolinium-enhanced MR serves as a marker for nerve root pathology in the unoperated lumbosacral spine, which may have clinical relevance in certain clinical situations [20].

Gene context of Blood-Nerve Barrier

• We investigated whether TM is present within human nerve and differentially expressed according to vessel caliber and proximity to the blood-nerve barrier [3].
• Permeability at the blood-brain and blood-nerve barriers of the neurotrophic factors: NGF, CNTF, NT-3, BDNF [21].
• Mutations in neurexin IV, contactin, and neuroglian result in the disruption of blood-nerve barrier function in the PNS, and ultrastructural analyses of the mutant embryonic peripheral nerves show loss of glial SJs [22].
• Gliotactin (Gli) is a cholinesterase-like molecule that is necessary for blood-nerve barrier integrity, and may, therefore, contribute to SJ development or function [23].
• These results indicate that the breakdown and following recovery of the blood-nerve barrier are closely associated with changes in the expression of claudins, occludin, VE-cadherin, and connexin43 and that the recovery time course is similar but nonidentical [24].

References