June 2017
Volume 58, Issue 8
Open Access
ARVO Annual Meeting Abstract  |   June 2017
Hypoxia protects horizontal cells from low glucose-induced Ca2+ dysregulation in the anoxia-tolerant goldfish
Author Affiliations & Notes
  • Michael William Country
    Department of Biology, University of Ottawa, Ottawa, Ontario, Canada
  • Benjamin F. N. Campbell
    Department of Biology, University of Ottawa, Ottawa, Ontario, Canada
  • Michael G. Jonz
    Department of Biology, University of Ottawa, Ottawa, Ontario, Canada
  • Footnotes
    Commercial Relationships   Michael Country, None; Benjamin F. N. Campbell, None; Michael G. Jonz, None
  • Footnotes
    Support  NSERC Grant 342303
Investigative Ophthalmology & Visual Science June 2017, Vol.58, 5187. doi:
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      Michael William Country, Benjamin F. N. Campbell, Michael G. Jonz; Hypoxia protects horizontal cells from low glucose-induced Ca2+ dysregulation in the anoxia-tolerant goldfish. Invest. Ophthalmol. Vis. Sci. 2017;58(8):5187.

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

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Abstract

Purpose : Intracellular Ca2+ concentration [Ca2+]i rises in neurons during ischemia or hypoxia, and induces cell death. The retina of anoxia-tolerant fish from the genus Carassius is resistant to hypoxia, but the underlying mechanisms at the cell level have not been investigated. Horizontal cells (HCs) of goldfish (C. auratus) exhibit spontaneous Ca2+ action potentials (APs), which may provide insights into HC Ca2+ dynamics during ischemia in the anoxia-tolerant retina. We tested the hypotheses that during hypoxia or ischemia Ca2+ APs in goldfish are reduced, and baseline [Ca2+]i is maintained, in a novel in vitro model.

Methods : Dissociated HCs were loaded with the Ca2+ indicator, Fura-2, and superfused for 40 min with HEPES-buffered extracellular solution (ECS). HCs were treated for 20 min with hypoxic ECS (N=6), glucose-free ECS (N=6), oxygen-glucose-deprivation (OGD) ECS (N=10), or no treatment (N=10). Baseline [Ca2+]i was monitored and spontaneous Ca2+ transients were analyzed for amplitude, time-to-peak, area-under-the-curve (AUC), duration, and frequency. The fold-change for each parameter was obtained by normalizing data to pre-application values. The Kruskal-Wallis test and Dunn’s post test were used for statistical analysis. Means ± S.E.M. are presented.

Results : Baseline [Ca2+]i was significantly higher following administration of 0 glucose ECS, and was 3.2±0.6-fold higher than controls (p<0.01). Interestingly, when 0 glucose was combined with hypoxia during OGD application, baseline was unaffected. Hypoxia alone had no effect upon [Ca2+]i baseline. Moreover, AP frequency was significantly affected (p<0.05). 0 glucose ECS abolished APs in nearly all cells, but frequency was preserved in hypoxic (p<0.05) and OGD conditions (p<0.05) over 0 glucose ECS. No significant changes in other parameters were observed.

Conclusions : Our results are consistent with the hypothesis that [Ca2+]i baseline is maintained in OGD and hypoxic conditions, but do not support the hypothesis that Ca2+ APs are down-regulated in hypoxic or OGD conditions. The data suggest that glucose deprivation (which occurs during ischemia) causes Ca2+ dysregulation in goldfish HCs, but hypoxia preserves low [Ca2+]i in spite of the concurrent low-glucose challenge. Further research will be needed to clarify the mechanisms by which hypoxia maintains Ca2+ homeostasis in the anoxia-tolerant goldfish.

This is an abstract that was submitted for the 2017 ARVO Annual Meeting, held in Baltimore, MD, May 7-11, 2017.

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