May 2008
Volume 49, Issue 13
Free
ARVO Annual Meeting Abstract  |   May 2008
Neuroprotective Effect of the Ketone Bodies Acetoacetate and β-hydroxybutyrate on Retinal Ganglion Cells in a Rat Model of NMDA Toxicity
Author Affiliations & Notes
  • T. J. Choragiewicz
    Centre for Ophthalmology, University of Tuebingen, Tuebingen, Germany
    Tadeusz Krwawicz Chair of Ophthalmology and 1st Eye Hospital, Medical University, Lublin, Poland
  • S. Thaler
    Centre for Ophthalmology, University of Tuebingen, Tuebingen, Germany
  • F. Schuettauf
    Centre for Ophthalmology, University of Tuebingen, Tuebingen, Germany
  • R. Rejdak
    Centre for Ophthalmology, University of Tuebingen, Tuebingen, Germany
    Tadeusz Krwawicz Chair of Ophthalmology and 1st Eye Hospital, Medical University, Lublin, Poland
  • E. Zrenner
    Centre for Ophthalmology, University of Tuebingen, Tuebingen, Germany
  • T. Zarnowski
    Tadeusz Krwawicz Chair of Ophthalmology and 1st Eye Hospital, Medical University, Lublin, Poland
  • Footnotes
    Commercial Relationships  T.J. Choragiewicz, None; S. Thaler, None; F. Schuettauf, None; R. Rejdak, None; E. Zrenner, None; T. Zarnowski, None.
  • Footnotes
    Support  Tistou und Charlotte Kerstan Stiftung and KFG (Zr-1/17-1)
Investigative Ophthalmology & Visual Science May 2008, Vol.49, 5502. doi:https://doi.org/
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      T. J. Choragiewicz, S. Thaler, F. Schuettauf, R. Rejdak, E. Zrenner, T. Zarnowski; Neuroprotective Effect of the Ketone Bodies Acetoacetate and β-hydroxybutyrate on Retinal Ganglion Cells in a Rat Model of NMDA Toxicity. Invest. Ophthalmol. Vis. Sci. 2008;49(13):5502. doi: https://doi.org/.

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

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Abstract

Purpose: : Ketone bodies (acetoacetate and beta-hydroxybutyrate) produced endogenously during starvation have been shown to exhibit neuroprotective and antiepileptic properties in models of brain ischemia and experimental epilepsy. Aim of this study was to investigate neuroprotective properties of systemic applicated lithium acetoacetate or sodium beta-hydroxybutyrate after N-methyl-D-aspartate (NMDA) damage of rat retinal ganglion cells.Material and

Methods: : Brown-Norway rats were used for the study. Lithium acetoacetate in two doses (250 mg/kg body weight (bw) and 62.5mg/kg bw [¼ dose]) and sodium beta-hydroxybutyrate in molar equivalent of the lithium acetoacetate doses (291.2 mg/kg bw and 72.8 mg/kg bw [¼ dose]) or phosphate buffer saline as control were administered intraperitoneally once a day for 21 consecutive days. On day 14 animals received intraocular NMDA (2 µl of 10mmol/l solution in PBS). On day 19 retinal ganglion cells were labeled retrogradely with Fluorogold. 2 days later rats were sacrificed, retinas were flatmounted and numbers of retinal ganglion (cells per mm2) were counted and compared to controls.

Results: : Retinal ganglion cell numbers in retinas from animals treated with lithium acetoacetate or sodium beta-hydroxybutyrate in full doses were significantly higher (48.4% and 41.5% increases, respectively; P<0.001, ANOVA) than in those treated with PBS. However, ¼ doses of both substances turned out to be ineffective.

Keywords: neuroprotection • cell survival • excitatory amino acid receptors 
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