Regulation of [3H] d-Aspartate Release from Mammalian Isolated Retinae by Hydrogen Sulfide
Hydrogen sulfide (H2S), can produce pharmacological effects on neural and non-neural tissues from several mammalian species. The present study investigates the pharmacological action of H2S, (using sodium hydrosulfide, NaHS, and/or sodium sulfide, Na2S as donors) on amino acid neurotransmission (using [3H] d-aspartate as a marker for glutamate) from isolated, superfused bovine and porcine retinae. Isolated neural retinae were incubated in Krebs solution containing [3H] d-aspartate at 37°C. Release of [3H] d-aspartate was elicited by high potassium (K+ 50 mM) pulse. Both NaHS and Na2S donors caused an inhibition of K+-evoked [3H] d-aspartate release from isolated bovine retinae without affecting basal [3H] d-aspartate efflux yielding IC50 values of 0.006 and 6 μm, respectively. Furthermore, NaHS inhibited depolarization-evoked release of [3H] d-aspartate from isolated porcine retinae with an IC50 value of 8 μM. The inhibitory action of NaHS on [3H] d-aspartate release from porcine retinae was blocked by propargyglycine, a selective inhibitor of cystathionine γ-lyase (CSE). Our results indicate that H2S donors can inhibit amino acid neurotransmission from both isolated bovine and porcine retinae, an effect that is dependent, at least in part, on intramural biosynthesis of H2S.
KeywordsHydrogen sulfide [3H] d-aspartate Retina Neurotransmission
We acknowledge the expert secretarial assistance of Ms. Carolyn Wahl (University of Houston) in the preparation of this manuscript.
- 12.Yap S, Naughten ER, Wilcken B, Wilcken DE, Boers GH (2000) Vascular complications of severe hyperhomocysteinemia in patients with homocystinuria due to cystathionine beta-synthase deficiency: effects of homocysteine-lowering therapy. Semin Thromb Hemost 26:335–340. doi: 10.1055/s-2000-8100 PubMedCrossRefGoogle Scholar
- 27.Opere CA, Monjok EM, Kulkarni KH, Zhao M, WeiDong Z, Ohia SE (2005) Regulation of [3H] d-aspartate release from mammalian isolated retinae by hydrogen sulfide. Invest Ophthalmol Vis Sci 46:E-Abstract 2228Google Scholar
- 32.Beltowski J (2004) Hydrogen sulfide as a biologically active mediator in the cardiovascular system. Postepy Hig Med Dosw (Online) 58:285–291Google Scholar
- 36.Guidotti TL (1996) Hydrogen sulphide. Occup Med (Lond) 46:367–371Google Scholar
- 44.Fiorucci S, Antonelli E, Distrutti E, Rizzo G, Mencarelli A, Orlandi S, Zanardo R, Renga B, Di SM, Morelli A, Cirino G, Wallace JL (2005) Inhibition of hydrogen sulfide generation contributes to gastric injury caused by anti-inflammatory nonsteroidal drugs. Gastroenterology 129:1210–1224PubMedCrossRefGoogle Scholar