May 2006
Volume 47, Issue 13
Free
ARVO Annual Meeting Abstract  |   May 2006
Retinal Ischaemia Results In A Preferential Loss Of Cone Components
Author Affiliations & Notes
  • D. Sun
    Department of Optometry and Vision Science, University of Auckland, Auckland, New Zealand
  • B. Bui
    Department of Optometry and Vision Sciences, University of Melbourne, Melbourne, Australia
  • M. Kalloniatis
    Department of Optometry and Vision Science, University of Auckland, Auckland, New Zealand
  • A. Vingrys
    Department of Optometry and Vision Sciences, University of Melbourne, Melbourne, Australia
  • Footnotes
    Commercial Relationships  D. Sun, None; B. Bui, None; M. Kalloniatis, None; A. Vingrys, None.
  • Footnotes
    Support  FoRST scholarship, AMRF, NZOVRF
Investigative Ophthalmology & Visual Science May 2006, Vol.47, 887. doi:
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      D. Sun, B. Bui, M. Kalloniatis, A. Vingrys; Retinal Ischaemia Results In A Preferential Loss Of Cone Components . Invest. Ophthalmol. Vis. Sci. 2006;47(13):887.

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Abstract

Purpose: : We investigated bipolar cell function secondary to retinal ischaemia to determine if there was a preferential effect on either the rod or cone ON and OFF bipolar cell pathways.

Methods: : Ischaemia was achieved by cannulating the anterior chamber with a 30–gauge needle attached to an elevated saline reservoir. Intraocular pressure was raised to 120 mmHg for 90 minutes, followed by 2 days of reperfusion. Glutamate receptor signaling was tracked by in vivo excitation mapping with the cation channel permeant probe agmatine (AGB; Marc et al., 2005 Vision Research). AGB permeates activated glutamate receptor channels in an activity dependent manner, and can be colocalized with a range of macromolecular markers. Excitation mapping with AGB enables simultaneous sampling of the integrated intrinsic excitation histories of all retinal neurons, and was colocalized with a range of macromolecular markers. To assess cone/rod bipolar cell function, full field electroretinograms (ERG) were recorded simultaneously from treated and control eyes 2 days post–ischaemia (n = 12). Scotopic ERG signals were collected using a single flash (–5.01 to 1.66 log.cd.s/m2, mixed rod/cone response), or a twin flash paradigm (1.66 log.cd.s/m2, interstimulus interval, 0.8 s) to isolate cone responses. Rod signals were derived by digital subtraction of cone signals from the mixed waveform.

Results: : Compared to control retina, ischaemia caused a marked reduction in AGB labelling, particularly within the inner nuclear layers. Colocalization patterns of AGB with PKC–alpha or Go–alpha indicated a selective loss of AGB labeling within both ON and OFF cone bipolar cells. Kainate activated AGB labelling confirmed the paucity of OFF cone bipolar cells. Ischaemia caused a severe loss in post–receptoral ERG components. A–wave and oscillatory potential amplitudes were reduced by 55 ± 8% and 88 ± 2%, respectively. The twin flash paradigm revealed a selective reduction in cone P2 amplitudes (97 ± 1%), compared with rod P2 amplitudes (73 ± 8%).

Conclusions: : Anatomical and functional results confirm a selective post–receptoral cone pathway dysfunction secondary to acute retinal ischaemia.

Keywords: ischemia • retina: proximal (bipolar, amacrine, and ganglion cells) • excitatory neurotransmitters 
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