June 2015
Volume 56, Issue 7
Free
ARVO Annual Meeting Abstract  |   June 2015
Regulation of Glutamate-Induced Excitotoxicity in Bovine Neural Retina by L-cysteine and Anandamide
Author Affiliations & Notes
  • Leah Mitchell
    Pharmaceutical Sciences, Texas Southern Unversity, Houston, TX
  • Oluwaseyi Fasiku
    Pharmaceutical Sciences, Texas Southern University, Houston, TX
  • Jenaye Robinson
    Pharmaceutical Sciences, Texas Southern University, Houston, TX
  • Catherine A Opere
    Pharmacy Sciences, Creighton University, Omaha, NE
  • Sunny E Ohia
    Pharmaceutical Sciences, Texas Southern University, Houston, TX
  • Ya Fatou Njie-Mbye
    Pharmaceutical Sciences, Texas Southern University, Houston, TX
  • Footnotes
    Commercial Relationships Leah Mitchell, None; Oluwaseyi Fasiku, None; Jenaye Robinson, None; Catherine Opere, None; Sunny Ohia, None; Ya Fatou Njie-Mbye, None
  • Footnotes
    Support None
Investigative Ophthalmology & Visual Science June 2015, Vol.56, 4399. doi:
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      Leah Mitchell, Oluwaseyi Fasiku, Jenaye Robinson, Catherine A Opere, Sunny E Ohia, Ya Fatou Njie-Mbye; Regulation of Glutamate-Induced Excitotoxicity in Bovine Neural Retina by L-cysteine and Anandamide. Invest. Ophthalmol. Vis. Sci. 2015;56(7 ):4399.

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

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Abstract

Purpose: There is evidence that hydrogen sulfide (H2S) and endocannabinoids can protect the central nervous system against glutamate-induced excitotoxicity and oxidative stress. In the present study, we will compare the neuroprotective actions of H2S (using L-cysteine as a substrate) and endocannabinoids (using anandamide) against glutamate-induced excitotoxicity in the isolated bovine retinae.

Methods: Isolated bovine neural retinae were pretreated with L-cysteine (10 nM - 1 µM) or anandamide (1 nM -100 nM) prior to insult with glutamate (2 mM), and retinal neuron survival was assessed using the methylthiazolydiphenyl-tetrazolium bromide (MTT) assay. For studies aimed at determining the involvement of the H2S biosynthesis pathway, glutamate-induced neurotoxic retinas were pretreated with enzyme inhibitors for H2S biosynthesis [aminooxyacetic acid (AOA, 30 µM), DL-propargylglycine (PAG, 1 mM), and ketobutyric acid (KBA, 1 mM)], prior to application of L-cysteine (100 nM).

Results: In the presence of glutamate (2 mM), only 68% of neurons survived when compared to control. The H2S substrate L-cysteine (100 nM) significantly (P<0.001) reversed glutamate (2 mM)-induced neuron degeneration. Interestingly, the H2S biosynthetic enzyme inhibitors, AOA, PAG, and KBA did not alter the neuroprotective effects of L-cysteine. Anandamide (1 nM - 10 nM) also completely prevented the glutamate (2 mM)-induced damage.

Conclusions: Both L-cysteine and anandamide can protect bovine neural retina from glutamate-induced excitotoxicity with the endocannabinoid displaying a higher potency. However, the neuroprotective effect of L-cysteine does not involve de novo intramural biosynthesis of H2S.<br />

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