Key result
Hydrogen sulfide elevates intracellular calcium in rat medullary neurons by increasing influx and mobilizing stores.
Hydrogen sulfide regulates intracellular calcium in primary rat medullary neurons by promoting both calcium influx and release from intracellular stores.
Should not yet change practice; leaves open H2S modulation of medullary neuronal calcium for further study.
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.
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Liu et al. (2016) studied this question. Hydrogen Sulfide (H2S) was evaluated on Intracellular calcium level ([Ca2+]i). Exogenous and endogenous hydrogen sulfide elevated intracellular calcium levels in primarily cultured rat medullary neurons by increasing calcium influx and mobilizing intracellular stores.
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