June 2020
Volume 61, Issue 7
Free
ARVO Annual Meeting Abstract  |   June 2020
Restoration of Light-evoked Electrical Signals in the Postmortem Mouse and Human Retina
Author Affiliations & Notes
  • Fatima Abbas
    University of Utah, Salt Lake City, Utah, United States
  • Silke Becker
    University of Utah, Salt Lake City, Utah, United States
  • Bryan W Jones
    University of Utah, Salt Lake City, Utah, United States
  • Anne M Hanneken
    2. Department of Molecular and Experimental Medicine, The Scripps Research Institute, San Diego, California, United States
  • Frans Vinberg
    University of Utah, Salt Lake City, Utah, United States
  • Footnotes
    Commercial Relationships   Fatima Abbas, None; Silke Becker, None; Bryan Jones, None; Anne Hanneken, None; Frans Vinberg, None
  • Footnotes
    Support  R00 EY026651 (FV), IRRF (FV), R01 EY015128 (BWJ), R01 EY028927 (BWJ), P30 EY014800 (BWJ Core Grant) and an Unrestricted Research Grant from Research to Prevent Blindness, New York, NY to the Department of Ophthalmology & Visual Sciences, University of Utah.
Investigative Ophthalmology & Visual Science June 2020, Vol.61, 3987. doi:
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    • Get Citation

      Fatima Abbas, Silke Becker, Bryan W Jones, Anne M Hanneken, Frans Vinberg; Restoration of Light-evoked Electrical Signals in the Postmortem Mouse and Human Retina. Invest. Ophthalmol. Vis. Sci. 2020;61(7):3987.

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

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Abstract

Purpose : Light-evoked responses of neurons in the retina disappear quickly after death. The mechanisms for the postmortem decay of light signals or under what conditions they can be restored ex vivo are not well understood. Here, we elucidate mechanisms leading to a loss of transduction and transmission of light signals and determine conditions that enable restoration of photoreceptor light signaling in the mouse and human retina.

Methods : We carried out in vivo and ex vivo Electroretinogram (ERG) recordings on mice postmortem (PM). For ex vivo ERGs, retinas were enucleated at several time-points PM. To understand the effects of PM acidosis and hypoxia, media pH or O2 were reduced in some of the experiments. Computational Molecular Phenotyping (CMP) analysis was carried out on mouse retinas fixed at 0 and 45min PM. We obtained research donor human eyes (Lion’s Eye Bank, UT) enucleated and delivered within 2.5-5 hrs PM, and measured light-evoked activity from retina samples using ex vivo ERG.

Results : Photoreceptor (PR) and bipolar cell (BC) responses were lost within ~10 min after death in vivo. However, rod and cone PR responses could be recorded from eyes enucleated up to 3 or 5-6 hrs PM in mouse and human retinas, respectively. BC component of the ex vivo ERG was observed only in one (out of 17) human donor retinas and decayed faster than the PR response in mouse experiments. CMP showed retinal cells show a loss of glutamate and glutamine within 45 min post mortem. Decrease of pH (to 6.8) caused a decay of BC response amplitudes in ex vivo ERG similar to that observed in in vivo whereas lowering of O2 to ~5-10% did not affect light responses during a ~20 min experiment. The maximal light responses of macular cones (Rmax) were significantly larger in donors who died of stroke compared to those who died due to cardiac arrest, while sepsis as a cause of death predicted the smallest Rmax.

Conclusions : We demonstrate that photoreceptor light responses that were lost quickly after death in vivo can be restored from mouse and human eyes enucleated several hours post mortem under ex vivo. We show that in addition to post mortem enucleation delay, cause of death should be considered as an important criteria for accepting donors. While research donors will allow studies of photoreceptor physiology, functional studies of the inner retina will probably require a use of eyes enucleated in less than one hour post mortem.

This is a 2020 ARVO Annual Meeting abstract.

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