June 2013
Volume 54, Issue 15
Free
ARVO Annual Meeting Abstract  |   June 2013
Further Studies On The Role Of Arachidonic Acid Metabolites In The Regulation Of Potassium-Induced [3H]D-Aspartate Release From Isolated Bovine Retinae By 5-epi-5-F3t-Isoprostane
Author Affiliations & Notes
  • Jamal Jamil
    Creighton.edu, Omaha, NE
  • Pratik Bankhele
    Creighton.edu, Omaha, NE
  • Ankita Salvi
    Creighton.edu, Omaha, NE
  • Thierry Durand
    Universities of Montpellier I and II, Montpellier cedex, France
  • Jean Galano
    Universities of Montpellier I and II, Montpellier cedex, France
  • Alexandre Guy
    Universities of Montpellier I and II, Montpellier cedex, France
  • Ya Fatou Njie-Mbye
    Texas Southern University, Houston, TX
  • Sunny Ohia
    Texas Southern University, Houston, TX
  • Catherine Opere
    Creighton.edu, Omaha, NE
  • Footnotes
    Commercial Relationships Jamal Jamil, None; Pratik Bankhele, None; Ankita Salvi, None; Thierry Durand, None; Jean Galano, None; Alexandre Guy, None; Ya Fatou Njie-Mbye, None; Sunny Ohia, None; Catherine Opere, None
  • Footnotes
    Support None
Investigative Ophthalmology & Visual Science June 2013, Vol.54, 6315. doi:
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      Jamal Jamil, Pratik Bankhele, Ankita Salvi, Thierry Durand, Jean Galano, Alexandre Guy, Ya Fatou Njie-Mbye, Sunny Ohia, Catherine Opere; Further Studies On The Role Of Arachidonic Acid Metabolites In The Regulation Of Potassium-Induced [3H]D-Aspartate Release From Isolated Bovine Retinae By 5-epi-5-F3t-Isoprostane. Invest. Ophthalmol. Vis. Sci. 2013;54(15):6315.

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

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Abstract

Purpose: We have evidence that eicosapentanoic acid (EPA)-derived F3-isoprostane (F3-IsoP), 5-epi-5-F3t-IsoP inhibits excitatory amino acid neurotransmitter release in bovine retina. In the present study, we investigated the role of arachidonic acid metabolites in the inhibitory action of 5-epi-5-F3t-IsoP on K+-induced [3H]D-aspartate release from bovine retina, in vitro.

Methods: Isolated neural retina were incubated in oxygenated Krebs solution containing 200 nM of [3H]D-aspartate and then prepared for studies of neurotransmitter release. Release of [3H]D-aspartate was evoked by K+ (50 mM) stimuli applied at 90 mins (S1) and at 108 mins (S2) after the onset of superfusion. F3-IsoP was added 8 min. before S1 while antagonists were present before and during S1 and S2.

Results: 5-epi-5-F3t-IsoP (0.1 nM - 0.1 µM) elicited an inhibitory action on K+-evoked [3H]D-aspartate release in a concentration-dependent manner, achieving a maximum inhibition of 46.9% at 0.1 µM (IC30 of 1 nM). Pretreatment of retinal tissues with the cyclooxygenase (COX) enzyme inhibitor, flurbiprofen (3 µM) unmasked a biphasic action, being inhibitory at lower (0.1 pM-10pM) and stimulatory at higher (0.1nM-0.1µM) concentrations of the IsoP. All the antagonists used exhibited no effect on K+-induced [3H]D-aspartate release. Similarly, SC 19220 (1 µM; EP1) and AH 6809 (10 µM; EP1-3/DP1) had no effect on 5-epi-5-F3t-IsoP (0.1 pM)-induced inhibition of the neurotransmitter release. On the contrary, other receptor antagonists, BAY-u3405 (10 µM; TP/DP), SQ 29548 (10 µM; TP) and ozagrel (10 µM; Tx-synthase) reversed the stimulatory action of the F3-IsoP (0.1 µM) on neurotransmitter release.

Conclusions: The EPA-metabolite, 5-epi-5-F3t-IsoP attenuates K+-induced [3H]D-aspartate release via COX enzyme-dependent mechanisms. Furthermore, the presence of COX unmasks a TP-dependent stimulatory action of this F3-IsoP on K+-induced [3H]D-aspartate release.

Keywords: 518 excitatory neurotransmitters • 675 receptors: pharmacology/physiology • 688 retina  
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