HYALURONIC-ACID IN THE NORMAL AND GLAUCOMATOUS OPTIC-NERVE

Eighteen normal human eye-bank eyes (age: 18-81 years), five fetal eye s (16-24 weeks), 11 primary open-angle glaucoma (POAG) eyes (age: 76-8 9 years), and two Schnabel's cavernous optic atrophy eyes were examine d using a biotinylated-hyaluronan binding protein to study the changes ih the distribution of hyaluronic acid (HA) in the fetal, adult and g laucomatous optic nerve head. The vitreous body served as a positive c ontrol. Sections treated with Streptomyces hyaluronidase were used to confirm specificity. Monoclonal antibodies to myelin basic protein (MB P) and glial fibrillary acidic protein (GFAP) were used as additional controls. In fetal optic nerve, HA was localized in blood vessels, per ipapillary sclera and the pial septae in the retrolaminar nerve. No st aining was associated with axons. Staining for MBP was negative. In ad ults, HA was found surrounding the myelin sheaths in the retrolaminar nerve; staining decreased with age. In contrast, HA staining in myelin ated peripheral nerves (e.g. ciliaries) remained unchanged with age. H A also was localized to the adventitia of arteries and veins throughou t the posterior segment. Compared to age-matched normal eyes, HA stain ing was virtually absent around myelin sheaths of the retrolaminar ner ve in POAG eyes. Similar changes were not found in other KA positive s tructures. In Schnabel's cavernous optic atrophy, HA was present in in creased amount in the atrophic area, but virtually absent in the remai ning retrolaminar nerve. HA staining was invariably positive in vitreo us, and Streptomyces hyaluronidase treated sections were negative. In adults, staining of MBP was associated with the myelin sheath in the r etrolaminar nerve. In contrast to HA, staining of MBP was unchanged wi th age and in POAG. In Schnabel's atrophy, MBP staining disappeared on ly in the atrophic area. HA in the retrolaminar optic nerve appears to be associated with the space-filling matrix between myelin sheaths. H A is not present in the axon bundles prior to myelination of the optic nerve. HA in the retrolaminar optic nerve appears to decrease with ag e and is further reduced in POAG; however, corresponding changes are n ot found in MBP or in peripheral nerves. Perhaps, decreased amounts of HA is related to a higher susceptibility to elevated intraocular pres sure or to optic nerve atrophy. In Schnabel's cavernous optic atrophy, HA is present in increased amount only in the atrophic area while MBP is markedly decreased, suggesting in situ production of HA in areas o f optic nerve atrophy. (C) 1997 Academic Press Limited.