June 2013
Volume 54, Issue 15
Free
ARVO Annual Meeting Abstract  |   June 2013
Axonal Transport Disruption in Retinal Ganglion Cells Following Transient Increase in Intraocular Pressure
Author Affiliations & Notes
  • Andrea Nuschke
    Retina and Optic Nerve Research Laboratory, Dalhousie University, Halifax, NS, Canada
    Physiology and Biophysics, Dalhousie University, Halifax, NS, Canada
  • Xu Wang
    Retina and Optic Nerve Research Laboratory, Dalhousie University, Halifax, NS, Canada
    Physiology and Biophysics, Dalhousie University, Halifax, NS, Canada
  • Neil O'Leary
    Retina and Optic Nerve Research Laboratory, Dalhousie University, Halifax, NS, Canada
    Ophthalmology and Visual Sciences, Dalhousie University, Halifax, NS, Canada
  • Corey Smith
    Retina and Optic Nerve Research Laboratory, Dalhousie University, Halifax, NS, Canada
    Physiology and Biophysics, Dalhousie University, Halifax, NS, Canada
  • Balwantray Chauhan
    Retina and Optic Nerve Research Laboratory, Dalhousie University, Halifax, NS, Canada
    Ophthalmology and Visual Sciences, Dalhousie University, Halifax, NS, Canada
  • Footnotes
    Commercial Relationships Andrea Nuschke, None; Xu Wang, None; Neil O'Leary, None; Corey Smith, None; Balwantray Chauhan, None
  • Footnotes
    Support None
Investigative Ophthalmology & Visual Science June 2013, Vol.54, 5097. doi:
  • Views
  • Share
  • Tools
    • Alerts
      ×
      This feature is available to authenticated users only.
      Sign In or Create an Account ×
    • Get Citation

      Andrea Nuschke, Xu Wang, Neil O'Leary, Corey Smith, Balwantray Chauhan; Axonal Transport Disruption in Retinal Ganglion Cells Following Transient Increase in Intraocular Pressure. Invest. Ophthalmol. Vis. Sci. 2013;54(15):5097.

      Download citation file:


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

      ×
  • Supplements
Abstract
 
Purpose
 

Glial activation, changes in optic nerve head (ONH) structure, and disruption of axonal transport (AT) have all been associated with retinal ganglion cell (RGC) loss. The time-course of such changes is not fully understood. We examined AT following a transient ischemic injury induced by elevated intraocular pressure (IOP).

 
Methods
 

The right eye of Brown Norway rats was cannulated with a 30-gauge needle attached to a saline reservoir, raised to induce IOP of 120 mmHg. The left eye served as control. Elevated IOP was maintained for 90 (known to cause RGC loss) or 30 (known not to cause RGC loss) minutes. Retrograde and anterograde AT was tracked via injections of cholera-toxin β-subunit (CTB) Alexa488 conjugate immediately prior to IOP increase into the superior colliculus or vitreous, respectively. Rats were sacrificed following IOP increase after 3, 6 or 24 hours for anterograde AT analysis, and 3, 7 or 14 days for retrograde AT analysis. Average fluorescence of each experimental and control optic nerve (ON) was measured from confocal images of longitudinal sections along its entire length (see Figure). Data were analysed with a linear mixed-effects model. Loss of RGCs was quantified in retinal wholemounts with the RGC marker, Brn3a.

 
Results
 

A 90-minute increase in IOP caused a mean 98% (N=2) loss of RGCs at 7 days post high IOP, and retrograde accumulation of CTB in the ONH. In experimental ONs there was a mean 28% (N=12, P<0.001) decrease in retrograde AT and a mean 56% (N=12, P<0.001) decrease in anterograde AT compared to control ONs, with no significant effect of recovery time. Following 30-minutes IOP elevation, RGC loss was negligible (1.2%, N=2) and there was no evidence of blockade at the ONH. However, there was a mean 13% (N=12, P<0.001) decrease in retrograde AT and a mean 8% (N=12, P<0.001) decrease in anterograde AT. Like the 90-minute injury, changes in AT following 30-minutes IOP elevation showed no significant effect of recovery time.

 
Conclusions
 

Despite no meaningful RGC loss following 30-minutes of elevated IOP, there was significant blockade of both retrograde and anterograde AT evident in the ON. It is possible that AT blockade may not be the primary cause for RGC loss, or that the induced AT blockade did not reach the threshold for RGC death.

  
Keywords: 531 ganglion cells • 568 intraocular pressure • 629 optic nerve  
×
×

This PDF is available to Subscribers Only

Sign in or purchase a subscription to access this content. ×

You must be signed into an individual account to use this feature.

×