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 [H-3] d-aspartate as a marker for glutamate) from isolated, superfused bovine and porcine retinae. Isolated neural retinae were incubated in Krebs solution containing [H-3] d-aspartate at 37A degrees C. Release of [H-3] d-aspartate was elicited by high potassium (K+ 50 mM) pulse. Both NaHS and Na2S donors caused an inhibition of K+-evoked [H-3] d-aspartate release from isolated bovine retinae without affecting basal [H-3] d-aspartate efflux yielding IC50 values of 0.006 and 6 mu m, respectively. Furthermore, NaHS inhibited depolarization-evoked release of [H-3] d-aspartate from isolated porcine retinae with an IC50 value of 8 mu M. The inhibitory action of NaHS on [H-3] d-aspartate release from porcine retinae was blocked by propargyglycine, a selective inhibitor of cystathionine gamma-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.