Click on image to view larger version.
Figure 1. Calcium stores responsible for DEA/NO-induced [Ca2+]i rises in GABAergic neurons. Average changes in relative fluorescence intensity (F/F0) in GABAergic NTS neurons after administration of DEA/NO and antagonists of different Ca2+ stores. Left bar) Effect of DEA/NO shown for comparison. Pretreatment with 2-APB (an inhibitor of the IP3-sensitive Ca2+ release) failed to prevent the DEA/NO effect. Nifedipine (a putative inhibitor of the NAADP-sensitive channel) did not block DEA/NO-elicited Ca2+ release, although there was a clear tendency to reduce it. Blockade of cADPR/ryanodine-sensitive stores with 8-Br-cADPR (a cADPR antagonist) abolished the effect of DEA/NO on Ca2+ release. Thus, cADPR/ryanodine-sensitive stores are likely to be the primary source of NO-released Ca2+. *P < 0.05, **P < 0.01, compared with control (paired t test). ##P < 0.01, compared with group treated with DEA/NO alone, unpaired t test.
