【摘要】 目的 :研究KATP 开放剂埃他卡林 (iptkalim ,IPT)对高K+ 刺激PC12释放谷氨酸 (Glu)的影响及其作用机制。方法 :以培养的PC12细胞为模型细胞 ,应用HPLC法测定细胞培养液中Glu含量。结果 :IPT以浓度依赖方式抑制高K+ 刺激PC12细胞释放Glu ,格列苯脲 (Gli)增强高K+ 刺激PC12细胞释放Glu的效应 ,并部分逆转IPT的抑制效应。PKC抑制剂HA 10 0和钙调素 (CaM )拮抗剂三氟拉嗪不影响高K+ 刺激PC12细胞释放Glu ,也不拮抗Gli的增强效应。结论 :IPT抑制Glu释放与开放KATP 有关 ,Gli拮抗IPT的抑制效应并非由PKC或CaM信号传导途径介导。更多还原

【Abstract】 AIM: To study the effects and mechanisms of ATP-sensitive potassium channel (K ATP) opener iptkalim (IPT) on the glutamate release from cultured PC12 cells induced by high K+. METHODS: The glutamate release from cultured PC12 cells was measured by using HPLC combined with fluorescent detector analysis. RESULTS: Different concentrations of IPT ( 0.01, 0.10, 1.00, 10.0, 100 μmol·L -1) were shown to inhibit glutamate release from PC12 cells induced by high K+ in a concentration-dependent manner, and these inhibitory effects were partly reversed by K ATP blocker glibenclamide (Gli), an inhibitor of K ATP channel. Incubation with 1.00 μmol·L -1 Gli alone increased the glutamate release induced by high K+, but selective PKC inhibitor HA-100 and calmodulin (CaM) antagonist trifluoperazine failed to affect the increment of glutamate release. CONCLUSION: Inhibition of glutamate release by IPT is partly reversed by Gli, indicating that the effect of IPT is mediated by the opening of the K ATP channel; PKC and CaM are not involved in the increment of glutamate release by Gli. These results demonstrate that K ATP channel is implicated in modulating glutamate release.更多还原