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Glaucoma-inducing Procedure in an In Vivo Rat Model and Whole-mount Retina Preparation
Published on: March 12, 2016
Ischaemia in the Zinn-Haller circle and glaucomatous optic neuropathy in macaque monkeys
Mari Hiraoka1, Kenichi Inoue, Taihei Ninomiya
1Division of Brain Development and Neuroregeneration, Tokyo Metropolitan Institute of Medical Science, Setagaya-ku, Tokyo, Japan. mari9190@true.ocn.ne.jp
Aims:
To elucidate the morphological features of optic neuropathy in an ischaemic model of glaucoma in macaque monkeys.
Methods:
The regional degenerative process was investigated by experimentally occluding the paraoptic branches of the lateral short posterior ciliary artery, that is, the circle of Haller and Zinn, in 11 eyes. Morphological changes in nerve fibres in the lamina cribrosa were evaluated by histopathology, immunocytochemistry and angiography, and the findings were compared with those observed in an aged macaque with spontaneous glaucomatous optic neuropathy.
Results:
Retinal ganglion cell axons were grouped in bundles and traversed through pores in columns of the lamina cribrosa. The processes of astrocytes extended to the bundles, and capillaries branched in surrounding connective tissue from the circular arterioles. Experimental ischaemia induced time-dependent anoxic deterioration of phosphorylated fibres in the temporal arcuate zone, accompanied by glial proliferation. A monkey with spontaneous visual impairment had nerve fibre loss and gliosis with collagenous proliferation in the temporal hemisphere, suggesting glaucomatous neuropathy.
Conclusions:
Circulatory interference in the circle of Haller and Zinn caused time-dependent deterioration in the area where anoxic segmental degeneration is associated with pathogenesis of open-angle glaucoma.
