Abstract

Glaucoma is considered a group of neurodegenerative diseases that damage the optic disc and result in a reduction of the field of vision. High intraocular pressure-induced deformation of optic nerve head (ONH) may compress the optic nerve and affect axonal transport. This study aims to show experimental observations: the activated astrocytes under high intraocular pressure play an important role in compression of optic nerve and block of axonal transport. Four-week duration of ocular hypertension (more than 20[Formula: see text]mm Hg) rats induced by cauterizing of three episcleral vessels and administering a fluorouracil subconjunctival injection in the right eye were enrolled and the left eyes of all the rats were used as a self-control. The axonal transport of the optic nerve was examined by a confocal laser scanning microscope after intravitreally injecting rhodamine-[Formula: see text]-isothiocyanate. The morphology of the optic nerve head was examined by hematoxylin–eosin (HE) staining, immunofluorescence staining and transmission electron microscopy (TEM). The results showed transport of rhodamine-[Formula: see text]-isothiocyanate was blocked in the experimental group, and fluorescent dye accumulated around the ONH. The nucleus counts of the coronal section kidney-shaped area showed that the number of cell nucleus in experimental eye was more than that of the control according to the results of HE staining. The increased collagen fibers in ONH were observed. The density of the glial fibrillary acidic protein in experimental eyes was a little bit higher than that in the control group by quantify analysis of the expression. The obvious changes of microstructure of the ONH also were found according to the images of TEM. It can be concluded that the activated astrocytes might squeeze the optic nerve, likely leading to optic nerve distortion and axonal flow blockage.

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call

Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.