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Oxidative Medicine and Cellular Longevity
Volume 2016 (2016), Article ID 2735347, 10 pages
Research Article

Hydrogen Sulfide Regulates the [Ca2+]i Level in the Primary Medullary Neurons

1Department of Physiology and Pathophysiology, Shanghai Medical College, Fudan University, Shanghai 200032, China
2Department of Neurology, Huashan Hospital, Fudan University, Shanghai 200040, China
3Department of Neurosurgery, Huashan Hospital, Fudan University, Shanghai 200040, China
4The Cardiovascular and Metabolic Research Unit, Laurentian University, Sudbury, ON, Canada P3E 2C6

Received 23 June 2016; Revised 12 September 2016; Accepted 27 September 2016

Academic Editor: Marta C. Monteiro

Copyright © 2016 Xiaoni Liu et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


In the present study, we attempted to elucidate mechanisms for the regulation of intracellular calcium levels by H2S in primary rat medullary neurons. Our results showed that NaHS significantly increased the level of in rat medullary neurons in a concentration-dependent manner. L-Cysteine and SAM significantly raised the level of in the medullary neurons while HA and/or AOAA produced a reversal effect. In addition, L-cysteine and SAM significantly increased but HA and/or AOAA decreased the production of H2S in the cultured neurons. The elevation induced by H2S was significantly diminished by EGTA-Ca2+-free solutions, and this elevation was also reduced by nifedipine or nimodipine and mibefradil, suggesting the role of L-type and/or T-type Ca2+ channels. Moreover, the effect of H2S on level in neurons was significantly attenuated by BAPTA-AM and thapsigargin, suggesting the source of Ca2+. Therefore, we concluded that both exogenous and endogenous H2S elevates level in primarily cultured rat medullary neurons via both increasing calcium influx and mobilizing intracellular Ca2+ stores from ER.