Kato H, Gotoh H, Kajikawa M, Suto K
Department of Bioengineering, Faculty of Engineering, Soka University, Tokyo, Japan.
Brain Res. 1998 Jan 1;779(1-2):329-33. doi: 10.1016/s0006-8993(97)01232-8.
Intracellular magnesium concentration ([Mg2+]i) of cultured dorsal root ganglion (DRG) neurons was measured using the magnesium indicator Mag-Fura-2/AM. [Mg2+]i was 0.48 +/- 0.08 mM (mean +/- SEM, n = 23) at rest, and it increased 3-fold by depolarization with a 60-mM K+ solution. The [Mg2+]i increase was observed in the absence of extracellular Mg2+, but the increase disappeared in the absence of extracellular Ca2+. 50 microM cadmium or 100 microM verapamil, a Ca2+ channel blocker, also diminished the rise of [Mg2+]i. The additional measurement of an intracellular Ca2+ concentration ([Ca2+]i) indicated that the [Mg2+]i rise requires a threshold concentration of [Ca2+]i to be reached; above 60 nM. The present results indicate that depolarization induces a Ca2+-influx through voltage dependent Ca channels and this causes the release of Mg2+ from intracellular stores into the cytoplasm.
使用镁指示剂Mag-Fura-2/AM测量培养的背根神经节(DRG)神经元的细胞内镁浓度([Mg2+]i)。静息时[Mg2+]i为0.48±0.08 mM(平均值±标准误,n = 23),用60 mM K+溶液去极化后其增加了3倍。在无细胞外镁的情况下观察到[Mg2+]i增加,但在无细胞外钙的情况下增加消失。50 μM镉或100 μM维拉帕米(一种钙通道阻滞剂)也减少了[Mg2+]i的升高。细胞内钙浓度([Ca2+]i)的额外测量表明,[Mg2+]i升高需要达到阈值浓度的[Ca2+]i;高于60 nM。目前的结果表明,去极化通过电压依赖性钙通道诱导钙内流,这导致镁从细胞内储存释放到细胞质中。