Please use this identifier to cite or link to this item: https://doi.org/10.1016/j.neures.2009.09.1713
Title: Hydrogen sulfide regulates intracellular pH in rat primary cultured glia cells
Authors: Lu, M. 
Hu, G.
Choo, C.H.
Hu, L.-F. 
Tan, B.H.
Bian, J.-S. 
Keywords: Acidification
Glia cells
H2S
Na+-independent Cl-/HCO3-exchanger
Na+/H+exchanger
Issue Date: 2010
Source: Lu, M., Hu, G., Choo, C.H., Hu, L.-F., Tan, B.H., Bian, J.-S. (2010). Hydrogen sulfide regulates intracellular pH in rat primary cultured glia cells. Neuroscience Research 66 (1) : 92-98. ScholarBank@NUS Repository. https://doi.org/10.1016/j.neures.2009.09.1713
Abstract: Intracellular pH (pHi) plays an important role in the regulation of central nervous system function. In the present study, we examined whether hydrogen sulfide (H2S), a recently recognized neuromodulator, regulates pHi in rat primary cultured glia cells. pHi was measured with a fluorescent sensitive dye, BCECF-AM. Activities of Cl-/HCO3- exchanger and Na+/H+ exchanger were examined by assessing their capacities to load or extrude H+ upon NH4Cl pulse load. We found that NaHS, a H2S donor, decreased pHi in a concentration-dependent manner ranging from 10 to 200 μM in the primary cultured microglia. Blockade of the Cl-/HCO3- exchanger with, 4,4′-diisothiocyanatostilbene-2,2′-disulfonic acid (DIDS) or Na+/H+ exchanger with 5-N-methyl-N-isobutylamiloride (MIA) significantly attenuated the pHi-lowering effect of NaHS. Moreover, NaHS significantly increased the activity of Cl-/HCO3- exchanger but inhibited that of Na+/H+ exchanger. The pH regulatory effect of H2S was also observed in primary cultured astrocytes, but not in SH-SY5Y neuronal cells. In conclusion, we found for the first time that H2S induced intracellular acidification in glia cells via regulation of the activities of Cl-/HCO3- exchanger and Na+/H+ exchanger. The present study may provide new evidence for H2S to serve as a neuromodulator and offer a potential approach for the treatment of neurological diseases. © 2009 Elsevier Ireland Ltd and the Japan Neuroscience Society.
Source Title: Neuroscience Research
URI: http://scholarbank.nus.edu.sg/handle/10635/27223
ISSN: 01680102
DOI: 10.1016/j.neures.2009.09.1713
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