May 2006
Volume 47, Issue 13
Free
ARVO Annual Meeting Abstract  |   May 2006
Retinal Ischaemia Results In A Preferential Loss Of Cone Components
D. Sun; B. Bui; M. Kalloniatis; A. Vingrys
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 
© 2006, The Association for Research in Vision and Ophthalmology, Inc., all rights reserved. Permission to republish any abstract or part of an abstract in any form must be obtained in writing from the ARVO Office prior to publication.
Copyright © 2025 Association for Research in Vision and Ophthalmology.
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