Hydrogen Sulfide Regulates the [Ca(2+)](i) Level in the Primary Medullary Neurons

In the present study, we attempted to elucidate mechanisms for the regulation of intracellular calcium levels by H(2)S in primary rat medullary neurons. Our results showed that NaHS significantly increased the level of [Ca(2+)](i) in rat medullary neurons in a concentration-dependent manner. L-Cysteine and SAM significantly raised the level of [Ca(2+)](i) 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 H(2)S in the cultured neurons. The [Ca(2+)](i) elevation induced by H(2)S was significantly diminished by EGTA-Ca(2+)-free solutions, and this elevation was also reduced by nifedipine or nimodipine and mibefradil, suggesting the role of L-type and/or T-type Ca(2+) channels. Moreover, the effect of H(2)S on [Ca(2+)](i) level in neurons was significantly attenuated by BAPTA-AM and thapsigargin, suggesting the source of Ca(2+). Therefore, we concluded that both exogenous and endogenous H(2)S elevates [Ca(2+)](i) level in primarily cultured rat medullary neurons via both increasing calcium influx and mobilizing intracellular Ca(2+) stores from ER.