Blood‐nerve barrier: ultrastructural and endothelial surface charge alterations following nerve crush

Abstract

Nerve crush results in an enhanced vascular permeability of the endoneurial vessels distal to the lesion. Vascular permeability at the blood-nerve barrier (BNB) to serum proteins is influenced by many factors, including anionic surface charge, endothelial vesicular transcytosis and the presence or absence of fenestrated vessels. Using mice and rats, the present ultrastructural investigation examined the effect of nerve crush (axonotmesis) on: (1) the distribution of endothelial anionic sites and (2) the appearance of fenestrations in endoneurial vessels after 4 and 14 day intervals as demonstrated with cationic probes. Transient anionic fenestrations developed in a minority of mouse endoneurial vessels in 4-day crushed nerves, but were not found in 14-day crushed nerves of mice nor in crushed nerves of rats. The known increase in the permeability of endoneurial vessels in rats and mice was not associated with reduced luminal labelling with cationic ferritin at physiological pH. At pH 2.0 the labelling of glycocalyx moieties (such as sialic acid) with cationic colloidal gold was disrupted in some epi- and endoneurial vessels of 4-day rats, but in a greater proportion after 14 days. The enhanced permeability of the BNB during degeneration and regeneration is related to the formation of anionic fenestrations in endoneurial vessels of mice and to the reduced and uneven distribution of endothelial glycocalyx moieties that are anionic at pH 2.0 in rats.