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Catherine A Opere, Pratik S Bankhele, Ankita A Salvi, Jamal Jamil, Dan Munt, Ya Fatou Njie-Mbye, Madhura Chitnis, Sunny E Ohia; Comparative inhibition of excitatory neurotransmission by N-Acetylcysteine and L-cysteine in bovine isolated retina. Invest. Ophthalmol. Vis. Sci. 2014;55(13):1886.
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© ARVO (1962-2015); The Authors (2016-present)
We have evidence that L-cysteine, the substrate for biosynthesis of hydrogen sulfide (H2S) can regulate potassium (K+)-evoked glutamate release from bovine isolated retina. However, the effect of the precursor for L-cysteine, N-acetyl cysteine (NAC) on excitatory neurotransmission has not been fully elucidated. In the present study, we compared the mechanisms by which L-cysteine and NAC regulate K+-evoked [3H] D-aspartate release and glutamate-induced neurotoxicity in bovine retina.
Isolated neural retina were incubated in oxygenated Krebs solution containing 200 nM of [3H] D-aspartate and then prepared for studies of neurotransmitter release. The MTT assay was used to assess retinal neuron survival.
Both L-cysteine (0.1 µM to 10 µM) and NAC (10 µM to 1 mM) attenuated K+-induced [3H] D-aspartate release in a concentration-dependent manner. At an equimolar concentration of 10 µM, L-cysteine and NAC inhibited evoked neurotransmitter release by 54.3% (p < 0.001) and 8.3%, respectively. Whereas, the CBS inhibitor, aminooxyacetic acid (AOA; 3mM) and the KATP channel blocker,glibenclamide (300 µM) had no effect on K+-induced [3H] D-aspartate release, they completely reversed the inhibitory effect of L-cysteine (1 µM to 10 µM). Interestingly, glibenclamide had no effect on NAC-induced inhibition of K+-induced [3H] D-aspartate release while AOA partially reversed this response. Both L-cysteine (1 mM) and NAC (1 µM) partially reversed glutamate (12 mM)-induced neuron degeneration by 31.1% (p<0.05) and 18.4%, respectively.
Both L-cysteine and NAC regulate excitatory neurotransmission in bovine retina by separate mechanisms.
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