Prejunctional Inhibitory Effects of Isoprostanes on Dopaminergic Neurotransmission in Bovine Retinae, In vitro

Liu, Hong; Zhao, Min; Opere, Catherine A.

doi:10.1007/s11064-007-9404-z

Cited by 5 publications

(9 citation statements)

References 31 publications

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“…Furthermore, pretreatment of bovine retinal tissues with COX-inhibitor, flurbiprofen attenuated IsoP-mediated inhibition of K ? -induced [ 3 H]dopamine release, suggesting the involvement of endogenously derived PGs in the IsoP response [19]. In other studies, we observed that the excitatory effect of 8-isoPGF 2a on K ?…”

Section: Discussionsupporting

confidence: 53%

“…In this study, 8-isoPGE 2 decreased both glutamate and glutamine, suggesting that the IsoP response was not likely due to an effect on the release of glutamate. Evidence from our laboratories demonstrates that IsoPs modulate retinal excitatory amino acid neurotransmitters and catecholamine release via an indirect action on COXand Tx synthase-pathways [19,20]. In the present study, we investigated the effect of COX-and Tx synthase inhibitors on the inhibitory effect of 8-isoPGE 2 on endogenous amino acid neurotransmitters.…”

Section: Discussionmentioning

confidence: 94%

“…Furthermore, IsoPs can modulate prejunctional acetylcholine [13] and norepinephrine release [14] in isolated guinea pig trachea cells and rat stomach, respectively. In ocular tissues, we have evidence that 8-isoPGE 2 can regulate the sympathetic neurotransmission in mammalian anterior uvea [17,18] and retina [19], in vitro. In addition, [20].…”

Section: Discussionmentioning

confidence: 95%

“…The vasoconstrictive effect of 8-iso-PGE 2 in human umbilical vein was reversed by both COX-inhibitors, indomethacin and NS-398 and the Tx-synthase inhibitor, furegrelate [12]. In bovine retina, the inhibitory effect of 8-isoPGE 2 on [ 3 H]dopamine release was reversed by the non-selective COX-enzyme inhibitor, flurbiprofen [19], in vitro. In addition to endogenous production of prostanoids, prostanoid TP and EP receptors have been implicated in the pharmacological effects of 8-isoPGE 2 .…”

Section: Introductionmentioning

confidence: 95%

“…Evidence from our laboratories demonstrate that 8-isoPGE 2 can regulate the release of exogenously applied [ 3 H]norepinephrine and [ 3 H]dopamine release in mammalian anterior uvea [17,18] and retina [19] respectively, in vitro. Furthermore, the IsoP attenuated K ?…”

Section: Introductionmentioning

confidence: 99%

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Role of Prostanoid Production and Receptors in the Regulation of Retinal Endogenous Amino Acid Neurotransmitters by 8-Isoprostaglandin E2, Ex Vivo

Zhao¹,

Destache²,

Ohia³

et al. 2009

Neurochem Res

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The role of enzymes and receptors of the prostanoid pathway in the inhibitory effect of 8-isoprostaglandin E2 (8-isoPGE2) on endogenous amino acid neurotransmitter levels was examined, ex vivo. Freshly isolated bovine eyeballs were injected intravitreally with IsoPs, incubated in Krebs buffer for 30 min and retina prepared for HPLC-ECD detection of amino acids. 8-isoPGE2 attenuated retinal glutamate and its metabolite, glutamine and glycine in a concentration-dependent manner. The nonselective cyclooxygenase (COX)-inhibitor, flurbiprofen, COX-2 selective inhibitor, NS-398 and thromboxane (Tx) synthase inhibitor, furegrelate had no effect on both basal amino acid levels and the inhibitory effects of 8-isoPGE2 (1-100 μM) on the retinal amino acids. Whereas the TP-receptor antagonist SQ-29548(10 μM) exhibited no effect, SC-19220(EP1; 30 μM), AH-6809(EP(1-3); 30 μM) and AH-23848(EP4; 30 μM) reversed the inhibitory effects of 8-isoPGE2 (0.01-100 μM) on glutamate, glutamine and glycine levels. We conclude that prostanoid EP-receptors regulate the inhibitory effect of 8-isoPGE2 on basal levels of endogenous amino acids in bovine retina, ex vivo.

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Section: Discussionsupporting

confidence: 53%

Section: Discussionmentioning

confidence: 94%

Section: Discussionmentioning

confidence: 95%

Section: Introductionmentioning

confidence: 95%

Section: Introductionmentioning

confidence: 99%

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Role of Prostanoid Production and Receptors in the Regulation of Retinal Endogenous Amino Acid Neurotransmitters by 8-Isoprostaglandin E2, Ex Vivo

Zhao¹,

Destache²,

Ohia³

et al. 2009

Neurochem Res

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Regulation of [3H]D-Aspartate Release by the 5-F2t-Isoprostane and Its 5-Epimer in Isolated Bovine Retina

et al. 2011

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We have evidence that 15-F₂-isoprostanes (15-F₂-IsoPs) regulate excitatory neurotransmitter release in ocular tissues. Although 5-F₂-IsoPs are abundantly produced in mammals, their pharmacological actions on neurotransmitter release remain unknown. In the present study, we compared the effect of the 5-F₂-IsoP epimer pair, 5-F(2t)-IsoP (C5-OH in β-position) and 5-epi-5-F(2t)-IsoP (C5-OH in α-position), on K⁺-evoked [³H]D-aspartate release in isolated bovine retina. We further examined the role of prostanoid receptors on the inhibitory action of 5-epi-5-F(2t)-IsoP on [³H]D-aspartate overflow. Isolated bovine retina were prepared for studies of K⁺-evoked release of [³H]D-aspartate using the superfusion method. 5-epi-5-F(2t)-IsoP (0.01 nM to 1 μM), attenuated K⁺-evoked [³H]D-aspartate release in a concentration-dependent manner, with the inhibitory effect of 26.9% (P < 0.001; IC₂₅ = 0.2 μM) being achieved at 1 μM concentration. Its 5-(S)-OH-epimer, 5-F(2t)-IsoP (0.1 nM-1 μM), exhibited an inhibitory biphasic action, yielding a maximal response of 35.7% (P < 0.001) at 10 nM concentration of the drug (IC₂₅ value of 3 nM). Although the prostanoid-receptor antagonists, AH 6809 (10 μM; EP₁₋₃/DP) and BAY-u3405 (10 μM; DP/Tx) exhibited no effect on 5-epi-5-F(2t)-IsoP (10 nM-1 μM)-mediated inhibition, SC-19220 (1 μM; EP₁) completely reversed 5-epi-5-F(2t)-IsoP (0.1 μM and 1 μM)-induced attenuation of K⁺-evoked [³H]D-aspartate release. Similarly, both SC-51322 (10 μM; EP₁ and AH 23848 (1 μM; EP₄) reversed the inhibitory action elicited by 5-epi-5-F(2t)-IsoP (0.1 μM) on the neurotransmitter release. We conclude that the 5-F₂-IsoP epimer pair, 5-F(2t)-IsoP and 5-epi-5-F(2t)-IsoP, attenuate K⁺-induced [³H]D-aspartate release in isolated bovine retina presumably via prostanoid receptor dependent mechanisms. The trans-orientation of the allylic hydroxyl group at position C5 accounts for the apparent biphasic response exhibited by 5-F(2t)-IsoP on excitatory neurotransmitter release.

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Role of the Non-enzymatic Metabolite of Eicosapentaenoic Acid, 5-epi-5-F3t-Isoprostane in the Regulation of [3H]d-Aspartate Release in Isolated Bovine Retina

et al. 2014

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We have evidence that F2-isoprostanes (F2-IsoPs) regulate the release of excitatory neurotransmitters in isolated bovine retina. Although 5-F3-IsoPs are generated in mammals, in vivo, their pharmacological actions on neurotransmitter release remain unknown. In this study, we investigated the effect of 5-epi-5-F3t-IsoP on K(+)-evoked [(3)H]D-aspartate release in isolated bovine retina using the superfusion method. Furthermore, we examined the role of arachidonic acid metabolites in the regulation of the neurotransmitter release by this novel IsoP. In the concentration range, 0.01 nM-0.1 µM, 5-epi-5-F3t-IsoP inhibited K(+)-evoked [(3)H]D-aspartate release in a concentration-dependent manner, achieving a maximum inhibition of 46.9 % at 0.1 µM (IC30 = 1 nM). The prostanoid receptor antagonists, AH 6809 (EP1-3/DP; 10 µM), SC 51322 (EP1; 10 µM) and SC 19220 (EP1; 1 µM) partially reversed 5-epi-5-F3t-IsoP-mediated inhibition of K(+)-induced [(3)H]D-aspartate release. Pretreatment of retinal tissues with the cyclooxygenase (COX) inhibitor, flurbiprofen (3 μM) unmasked a biphasic action of 5-epi-5-F3t-IsoP that was inhibitory at lower (0.1-10 pM) and stimulatory at higher concentrations (≥0.1 nM). The prostanoid pathway antagonists, BAY-u3405 (10 μM; TP/DP-receptors), SQ 29548 (10 μM; TP-receptor) and ozagrel (10 μM; Tx-synthase inhibitor) abolished the stimulatory action of the 5-epi-5-F3t-IsoP (0.1 μM) on neurotransmitter release. In conclusion, 5-epi-5-F3t-IsoP attenuates K(+)-induced [(3)H]D-aspartate release in a concentration-dependent manner by mechanisms that are partially dependent on activation of pre-junctional prostanoid EP1-receptors. Moreover, blockade of the COX-pathway unmasks a biphasic action for 5-epi-5-F3t-IsoP that is inhibitory at low concentrations and stimulatory at higher concentrations. Products of the thromboxane synthase pathway may partially account for the stimulatory action of this F3-IsoP on isolated bovine retina.

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Prejunctional Inhibitory Effects of Isoprostanes on Dopaminergic Neurotransmission in Bovine Retinae, In vitro

Cited by 5 publications

References 31 publications

Role of Prostanoid Production and Receptors in the Regulation of Retinal Endogenous Amino Acid Neurotransmitters by 8-Isoprostaglandin E2, Ex Vivo

Role of Prostanoid Production and Receptors in the Regulation of Retinal Endogenous Amino Acid Neurotransmitters by 8-Isoprostaglandin E2, Ex Vivo

Regulation of [3H]D-Aspartate Release by the 5-F2t-Isoprostane and Its 5-Epimer in Isolated Bovine Retina

Role of the Non-enzymatic Metabolite of Eicosapentaenoic Acid, 5-epi-5-F3t-Isoprostane in the Regulation of [3H]d-Aspartate Release in Isolated Bovine Retina

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