Abstract
Abstract: :
Evidence from our laboratory shows that hydrogen sulfide (H2S) can inhibit sympathetic neurotransmission from isolated porcine iris–ciliary bodies (Ohia et al., ARVO Abstract, 2005). Since relatively high concentrations of H2S in the brain has been associated with some neurological disorders such as Downs Syndrome (Kamoun et al., Am. J. Med. Gen. 116A:310, 2003), we considered the possibility that this gas may alter excitatory amino acid neurotransmission from mammalian retina. Purpose: To study the pharmacological actions of H2S (using sodium hydrosulfide, NaHS and sodium sulfide, Na2S as H2S donors) on potassium (K+)–depolarization evoked release of [3H]D–aspartate from bovine and porcine retinae, in vitro. Methods: Isolated bovine and porcine neural retinae were incubated in oxygenated Krebs solution containing 200nM of [3H]D–aspartate for 60 mins and then prepared for studies of neurotransmitter release using the superfusion method. Release of [3H]D–aspartate was evoked by iso–osmotic concentration of K+(50 mM) stimuli applied at 80–88 mins (S1) and 116–124 mins (S2) after the onset of superfusion. Results: Both NaHS (1 nM –1 µM) and Na2S (0.1–10 µM) produced a concentration–dependent inhibition of K+–evoked [3H]D–aspartate release from bovine and porcine retinae without affection basal tritium efflux. In general, NaHS was more potent than Na2S in eliciting inhibition of evoked [3H]D–aspartate overflow regardless of species examined. For instance, in bovine retinae, an equimolar concentration of NaHS and Na2S (100 nM) caused 40% and 15% inhibition of K+–induced [3H]D–aspartate release. An inhibitor of cystathionine ß–synthase, propargylglycine (1 mM) blocked the inhibitory response elicited by NaHS (1 nM) on K+–evoked [3H]D–aspartate release from porcine retinae. Conclusions: Both NaHS and Na2S can inhibit the release of K+–evoked [3H]D–aspartate release from bovine and porcine retinae, an action that is dependent on the production of H2S in these tissues. Further studies are needed to elucidate the mechanism of action of this gas on excitatory amino acid neurotransmission from mammalian retinae.
Keywords: excitatory neurotransmitters • retina • pharmacology