May 2003
Volume 44, Issue 13
ARVO Annual Meeting Abstract  |   May 2003
Disturbance of Ionic Homeostasis in Different In Vitro Models of Retinal Ischemia
Author Affiliations & Notes
  • A.V. Dmitriev
    Dept of Neurobiology, Univ of Alabama Sch of Med, Birmingham, AL, United States
  • S.C. Mangel
    Dept of Neurobiology, Univ of Alabama Sch of Med, Birmingham, AL, United States
  • Footnotes
    Commercial Relationships  A.V. Dmitriev, None; S.C. Mangel, None.
  • Footnotes
    Support  Grants from the NIH (EY005102) and NSF (IBN-9819981).
Investigative Ophthalmology & Visual Science May 2003, Vol.44, 2937. doi:
  • Views
  • Share
  • Tools
    • Alerts
      This feature is available to authenticated users only.
      Sign In or Create an Account ×
    • Get Citation

      A.V. Dmitriev, S.C. Mangel; Disturbance of Ionic Homeostasis in Different In Vitro Models of Retinal Ischemia . Invest. Ophthalmol. Vis. Sci. 2003;44(13):2937.

      Download citation file:

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

  • Supplements

Abstract: : Purpose: Ischemia severely disturbs ionic homeostasis in the brain, but its effects on ionic homeostasis in the retina have not been characterized. We thus examined how and to what extent the extracellular concentrations of the most physiologically important ions (K+, Ca2+, H+) in the in vitro retina are affected by ischemia and related neuron-damaging conditions. We focused on ischemia-dependent ionic changes in the photoreceptor layer because the type of ionic channels in the photoreceptor plasma membrane is greatly different from that in a typical brain neuron (e.g. photoreceptors have no voltage-dependent Na-channels, but have cGMP-regulated Na/Ca-channels). Methods: Extracellular ionic concentrations were measured with ion-selective microelectrodes in the rabbit eyecup preparation. Aglycemia, anoxia, and acidosis were mimicked by removing glucose from the superfusate, by replacing O2 with N2 in the gas mixture that bubbled the superfusate, and by replacing NaHCO3 with NaCl, respectively. Three in vitro models of ischemia were used: 1) oxygen-glucose deprivation (OGD), 2) the combination of OGD with acidosis, and 3) the cessation of superfusate flow. Results: Anoxia evoked a stronger disturbance of ionic homeostasis than aglycemia and acidosis, and a combination of all three had slightly stronger effects than anoxia alone. Light-induced activity in the outer retina was quickly eliminated under anoxia, but not under aglycemia or acidosis. The general pattern of ionic changes was similar in all of these conditions. For example, [K+]o in the photoreceptor layer increased (up to 10 mM) in the first minute, but then decreased and after 30 minutes was only 2-3 mM higher than the control level. In contrast, when the flow of superfusate was stopped, [K+]o in the photoreceptor layer (after an initial relatively small tri-phasic change during the first 4-5 minutes) increased, slowly and monotonically, with a rate of about 0.5 mM per min. After a 30-minute cessation in the flow of superfusate, distal [K+]o exceeded 20 mM, but photoreceptor cells were still able to respond to light. Conclusions: These findings indicate that cessation of superfusate flow alters retinal extracellular ionic homeostasis to a greater extent than models in which superfusion is continuous (i.e. OGD or OGD with acidosis). The findings also suggest that the disturbance of ionic homeostasis during ischemia or other neuron-damaging conditions can vary significantly depending on the type and number of ionic channels in the plasma membrane of the neuron under study.

Keywords: ischemia • hypoxia • pathology: experimental 

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.