Okuma Y, Osumi Y
Brain Res. 1986 Jan 15;363(1):47-52. doi: 10.1016/0006-8993(86)90657-8.
Effects of the absence of calcium on the KCl- and electrical stimulation-induced releases of endogenous dopamine (DA) from rat brain slices were studied and the findings were compared with the effects on the release of endogenous noradrenaline (NA). DA and NA were extracted by the aluminum-adsorption method and assayed electrochemically by high-performance liquid chromatography. KCl, 15 mM, induced a significant increase in the release of DA from both the striatum and the hypothalamus, even in the Ca2+-free medium containing 1 mM EGTA. In the normal medium, the KCl-induced release of DA was concentration-dependent (15, 30 and 50 mM), while that in the Ca2+-free medium showed a plateau at 30 mM of KCl. The release of DA induced by electrical stimulation (10 cycles/s, 2 ms, 30 mA, for 5 min) was abolished in the Ca2+-free medium as was NA induced by both KCl and electrical stimulation. Nomifensine, 10 microM, a DA transport inhibitor, abolished the 15 mM KCl-induced release of DA in the Ca2+-free medium. On the other hand, the release of DA induced by electrical stimulation was considerably enhanced by nomifensine. Therefore, the mode of DA release induced by KCl sometimes differed from that induced by electrical stimulation. The present results also suggest that DA released by KCl in the Ca2+-free medium originates from cytoplasmic DA storage sites, through a carrier-mediated process.
研究了无钙对大鼠脑片由氯化钾(KCl)和电刺激诱导的内源性多巴胺(DA)释放的影响,并将结果与对内源性去甲肾上腺素(NA)释放的影响进行比较。采用铝吸附法提取DA和NA,并通过高效液相色谱电化学法进行测定。即使在含有1 mM乙二醇双四乙酸(EGTA)的无钙培养基中,15 mM的KCl也能显著增加纹状体和下丘脑DA的释放。在正常培养基中,KCl诱导的DA释放呈浓度依赖性(15、30和50 mM),而在无钙培养基中,在30 mM KCl时出现平台期。无钙培养基中电刺激(10次/秒,2毫秒,30毫安,持续5分钟)诱导的DA释放被消除,KCl和电刺激诱导的NA释放也被消除。10 μM的诺米芬辛(一种DA转运抑制剂)消除了无钙培养基中15 mM KCl诱导的DA释放。另一方面,诺米芬辛显著增强了电刺激诱导的DA释放。因此,KCl诱导的DA释放模式有时与电刺激诱导的不同。目前的结果还表明,无钙培养基中KCl释放的DA通过载体介导的过程源自细胞质DA储存位点。