June 2013
Volume 54, Issue 15
ARVO Annual Meeting Abstract  |   June 2013
Further Studies on the Inhibition of [3H]D-Aspartate Release by Hydrogen Sulfide Donors in Isolated Bovine Retina
Author Affiliations & Notes
  • Pratik Bankhele
    Creighton University, Omaha, NE
  • Jamal Jamil
    Creighton University, Omaha, NE
  • Ankita Salvi
    Creighton University, Omaha, NE
  • Ya Fatou Njie-Mbye
    Texas Southern University, Houston, TX
  • Madhura Kulkarni
    Texas Southern University, Houston, TX
  • Sunny Ohia
    Texas Southern University, Houston, TX
  • Catherine Opere
    Creighton University, Omaha, NE
  • Footnotes
    Commercial Relationships Pratik Bankhele, None; Jamal Jamil, None; Ankita Salvi, None; Ya Fatou Njie-Mbye, None; Madhura Kulkarni, None; Sunny Ohia, None; Catherine Opere, None
  • Footnotes
    Support None
Investigative Ophthalmology & Visual Science June 2013, Vol.54, 6325. doi:
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      Pratik Bankhele, Jamal Jamil, Ankita Salvi, Ya Fatou Njie-Mbye, Madhura Kulkarni, Sunny Ohia, Catherine Opere; Further Studies on the Inhibition of [3H]D-Aspartate Release by Hydrogen Sulfide Donors in Isolated Bovine Retina. Invest. Ophthalmol. Vis. Sci. 2013;54(15):6325.

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      © ARVO (1962-2015); The Authors (2016-present)

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Purpose: We have previously reported that hydrogen sulfide (H2S) donors can regulate [3H]D-aspartate release in isolated mammalian. In the present study, we compared the effect of H2S-producing compounds on K+-induced glutamate release (using [3H]D-aspartate as a marker) in isolated bovine retina. Furthermore, we examined the mechanism underlying the inhibitory action of H2S-donors on K+-induced [3H]D-aspartate release in bovine retina. in bovine retina.

Methods: Isolated bovine retina were incubated for 60 min. at 37oC in carbogen-gassed Krebs buffer containing 200 nM of [3H]D-aspartate. Release of [3H]D-aspartate was elicited by iso-osmotic concentration of K+ (50mM)-stimuli applied at 80-88 min. (S1) and 116-124 min. (S2) after the onset of superfusion. H2S-donors were added 12-18 min. before S2 while antagonists were present before and during S1 and S2.

Results: The H2S-producing compounds, GYY 4137 (10 nM-10 µM), NaHS (1 nM-1 µM) and L-cysteine (1-10 µM) elicited a concentration-dependent inhibition of K+-induced [3H]D-aspartate release in isolated bovine retina. At an equimolar concentration (1 µM), the rank order of activity was as follows: L-cysteine > NaHS > GYY 4137. The substrate for endogenous H2S production, L-cysteine was most potent, eliciting a maximum inhibitory action of 54.2% (n=4; p<0.01) at the 10 µM concentration (IC50 of about 5 µM). Whereas, the cystathionine β-synthase inhibitor, aminooxyacetic acid (3 mM) and the ATP-sensitive potassium channel (KATP) inhibitor, glibenclamide (300 μM) had no effect (p>0.05) on K+-induced [3H]D-aspartate release, they both reversed the inhibitory action of GYY 4137 (10 μΜ) and L-cysteine (1-10 µM) on the neurotransmitter release. Furthermore, the nitric oxide (NO) synthase inhibitor, L-NAME (300 µM) reversed the inhibitory action of GYY 4137 (1-10 µM) on the excitatory neurotransmitter release.

Conclusions: KATP-channels, NO pathway and in situ production of H2S contribute to the inhibitory action of H2S-producing compounds on excitatory neurotransmitter release in isolated bovine retina.

Keywords: 518 excitatory neurotransmitters • 688 retina • 616 neurotransmitters/neurotransmitter systems  

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