June 2015
Volume 56, Issue 7
Free
ARVO Annual Meeting Abstract  |   June 2015
Dynein, Kinesin and Morphological Changes in Optic Nerve Axons in a Rat Model with Cerebrospinal Fluid Pressure Reduction
Author Affiliations & Notes
  • Qian Liu
    Beijing Institute of Ophthalmology, Beijing Tongren Hospital, Beijing, China
  • Zheng Zhang
    Beijing Institute of Ophthalmology, Beijing Tongren Hospital, Beijing, China
  • Ningli Wang
    Beijing Institute of Ophthalmology, Beijing Tongren Hospital, Beijing, China
  • Footnotes
    Commercial Relationships Qian Liu, None; Zheng Zhang, None; Ningli Wang, None
  • Footnotes
    Support None
Investigative Ophthalmology & Visual Science June 2015, Vol.56, 4133. doi:
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      Qian Liu, Zheng Zhang, Ningli Wang; Dynein, Kinesin and Morphological Changes in Optic Nerve Axons in a Rat Model with Cerebrospinal Fluid Pressure Reduction. Invest. Ophthalmol. Vis. Sci. 2015;56(7 ):4133.

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      © ARVO (1962-2015); The Authors (2016-present)

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Abstract

Purpose: To examine the influence of experimentally reduced cerebrospinal fluid pressure (CSFP) as compared to elevated intraocular pressure (IOP) on axonal morphology and motor proteins in retinal ganglion cells (RGCs).

Methods: The experimental study included30 rats which underwent cerebrospinal fluid drainage for 6 hours, 30 rats which unilaterally underwent IOP elevation for 6 hours, and 30 rats in a control group with changes neither in IOP nor CSFP. Six hours after baseline, the animals were sacrificed and the eyes were histologically and immunohistochemically examined.

Results: Both, in the high-IOP group and in the low-CSFP group as compared to the control group, RGC axons became abnormally dilated and accumulating vesicles. The high-IOP group and the low-CSFP group as compared to the control group showed immunohistochemically an accumulation of dynein IC at the optic nerve head and retina, a reduction in kinesin HC immunoreactivity in the optic nerve fiber axons. As a corollary, Western blot analysis showed an elevation of dynein IC protein levels in the optic nerve head and retina, and a decreases in kinesin HC protein levels in the optic nerve.

Conclusions: The results suggest that experimental models with an acute IOP rise or with an acute CSFP reduction showed similar morphologic changes in the retinal ganglion cell axons and similar immunohistochemical changes in the levels of the axonal motor proteins kinesin HC and dynein IC. It supports the hypothesis that disrupted axonal transport in RGC may be involved in the pathogenesis of optic neuropathy in normal-pressure glaucoma.

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