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首页> 外文期刊>Life sciences >Pharmacological characterization of the effects of methylmercury and mercuric chloride on spontaneous noradrenaline release from rat hippocampal slices.
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Pharmacological characterization of the effects of methylmercury and mercuric chloride on spontaneous noradrenaline release from rat hippocampal slices.

机译：甲基汞和氯化汞对大鼠海马切片自发去甲肾上腺素释放的影响的药理学表征。

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The environmental contaminants methylmercury (MeHg) and mercuric chloride (HgCl2) stimulated the spontaneous release of [3H]noradrenaline ([3H]NA) from hippocampal slices in a time- and concentration-dependent manner. Both MeHg and HgCl2 were similarly potent, with an EC50 of 88.4 microM and 75.9 microM, respectively. The releasing effects of MeHg and HgCl2 increased in the presence of desipramine, showing that the mechanism does not involve reversal of the transmitter transporter, and were completely blocked by reserpine preincubation, indicating a vesicular origin of [3H]NA release. The voltage-gated Na+ channel blocker tetrodotoxin (TTX) did not affect the response to mercury compounds. [3H]NA release elicited by MeHg was partially dependent on extracellular Ca2+, since it decreased significantly in a Ca2+-free EGTA-containing medium whereas HgCl2 induced a release of [3H]NA independent of extracellular Ca2+. Neither Ca2+-channels blockers, cobalt chloride (CoCl2) and (omega-conotoxin-GVIA, nor the Na+/Ca2+-exchanger inhibitor benzamil reduced MeHg-evoked [3H]NA release. Moreover, thapsigargin or caffeine, endoplasmic reticulum Ca2+-depletors, did not modify metal-evoked [3H]NA release, whereas ruthenium red, which inhibits the mitochondrial Ca2+ transport, decreased the effect of both MeHg and HgCl2. All these data indicate that, in hippocampal slices, mercury compounds release [3H]NA from the vesicular pool by a mechanism involving Ca2+ mobilization from mitochondrial stores.
机译：环境污染物甲基汞（MeHg）和氯化汞（HgCl2）刺激了海马片中[3H]去甲肾上腺素（[3H] NA）的自发释放，并具有时间和浓度依赖性。 MeHg和HgCl2的效价相似，EC50分别为88.4 microM和75.9 microM。在地昔帕明的存在下，MeHg和HgCl2的释放作用增强，表明该机制不涉及递质转运蛋白的逆转，并且被利血平预孵育完全阻止，表明[3H] NA释放的囊泡起源。电压门控的Na +通道阻断剂河豚毒素（TTX）不会影响对汞化合物的响应。 MeHg引起的[3H] NA释放部分取决于细胞外Ca2 +，因为在不含Ca2 +的含EGTA的培养基中，其显着降低，而HgCl2诱导了独立于细胞外Ca2 +的[3H] NA释放。 Ca2 +通道阻滞剂，氯化钴（CoCl2）和（ω-芋螺毒素-GVIA）或Na + / Ca2 +交换剂苯扎米尔均不降低MeHg诱发的[3H] NA释放。此外，毒胡萝卜素或咖啡因，内质网Ca2 +耗竭剂，不会改变金属诱发的[3H] NA释放，而抑制线粒体Ca2 +转运的钌红降低了MeHg和HgCl2的作用，所有这些数据表明，在海马切片中，汞化合物从通过从线粒体存储中动员Ca2 +的机制来形成囊泡池。

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