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Catherine A Opere, Jamal Jamil, Emily Kawesa-Bass, Thierry Durand, Alexandre Guy, Jean-Marie Galano, Ya Fatou Njie-Mbye, Jenaye Robinson, Sunny E Ohia; Regulation of Potassium-Induced [3H]D-Aspartate Release from Bovine Isolated Retina by the DHA-Metabolite , 4(S)-F4t-Neuroprostane: Role of Arachidonic Acid Metabolites. Invest. Ophthalmol. Vis. Sci. 2016;57(12):113.
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There is evidence that the free radical-derived, EPA metabolite, 5-epi-5-F3t-isoprostane regulates the release of excitatory neurotransmitters in isolated bovine retina (Jamil et al., 2014 Neurochem. Res. 39:2360-2369). However, the pharmacological role of analogous DHA metabolites on retinal neurons has not been fully elucidated. In the present study, we investigated the role of arachidonic acid metabolites in the regulation of K+-induced glutamate release (using [3H]D-aspartate as a marker) by 4(S)-F4t-neuroprostane (4(S)-F4t-NeuroP) in isolated bovine retina.
Freshly isolated bovine retina were incubated for 60 mins in carbogen-gassed Krebs buffer solution (pH 7.45; 37 degrees centigrade) containing 200nM of [3H]D-aspartate. Retinal tissues were placed in thermostatically controlled superfusion chambers and the release of [3H]D-aspartate was evoked by iso-osmotic concentration of K+ (50mM)-stimuli applied at 80-88 mins (S1) and 116-124 mins (S2) after the onset of superfusion. The DHA-metabolite, 4(S)-F4t-NeuroP was added to the buffer solution 15 mins before S2. When used, antagonists were added 10 mins before S2.
The DHA-metabolite, 4(S)-F4t-NeuroP (1 nM to 1 µM) enhanced K+-induced [3H]D-aspartate release from bovine retina, achieving a maximum response of 17%±1.01 (n=4; p<0.05) at 0.1 µM. Pretreatment with flurbiprofen (3 µM) unmasked a concentration-dependent inhibitory action of 4(S)-F4t-NeuroP, achieving an inhibition of 45.7%±3.7 (n=3; p<0.05) at the 1 µM concentration. Although the prostanoid antagonists, BAY-u3406 (ramatroban; DP2/TP; 10 µM), SQ 29548 (TP/DP; 10 µM), SC 51322 (EP1; 10 µM) and SC 19220 (EP1; 1 µM) had no effect on basal and K+-induced [3H]D-aspartate release, they completely reversed the inhibitory effect elicited by 4(S)-F4t-NeuroP (0.1 µM).
4(S)-F4t-NeuroP can exert both excitatory and inhibitory actions on K+-depolarization -induced release of [3H]D-aspartate from the bovine isolated retina. The excitatory effects of this neuroP is mediated, at least in part, by arachidonic acid metabolites.
This is an abstract that was submitted for the 2016 ARVO Annual Meeting, held in Seattle, Wash., May 1-5, 2016.
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