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首页> 外文期刊>Neurochemistry International: The International Journal for the Rapid Publication of Critical Reviews, Preliminary and Original Research Communications in Neurochemistry >Mechanism of action of methylmercury on in vivo striatal dopamine release. Possible involvement of dopamine transporter.
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Mechanism of action of methylmercury on in vivo striatal dopamine release. Possible involvement of dopamine transporter.

机译：甲基汞对体内纹状体多巴胺释放的作用机理。多巴胺转运蛋白可能参与其中。

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摘要

Methylmercury (MeHg) produces significant increases in the spontaneous output of dopamine (DA) from rat striatal tissue. The mechanism through MeHg produces such increase in the extracellular DA levels could be due to increased DA release or decreased DA uptake into DA terminals. One of the aims of this study was to investigate the role of DA transporter (DAT) in the MeHg-induced DA release. Coinfusion of 400 microM MeHg and nomifensine (50 microM) or amphetamine (50 microM) produced increases in the release of DA similar to those produced by nomifensine and amphetamine alone. In the same way, MeHg-induced DA release was not attenuated under Ca(2+)-free conditions or after pretreatment with reserpine (10 mg/kg i.p.) or tetrodotoxin (TTX), suggesting that the DA release was independent of calcium and vesicular stores, as well as it was not affected by the blockade of voltage sensitive sodium channels. Thus, to investigate whether depolarization of dopaminergic terminal was able to affect MeHg-induced DA release, we infused 75 mM KCl through the dialysis membrane. Our results clearly showed a decrease induced by MeHg in the KCl-evoked DA release. Taken together, these results suggest that MeHg induces release of DA via transporter-dependent, calcium- and vesicular-independent mechanism and it decreases the KCl-evoked DA release.
机译：甲基汞（MeHg）可明显增加大鼠纹状体组织中多巴胺（DA）的自发输出。通过MeHg产生的这种机制增加了细胞外DA的水平，这可能是由于DA释放增加或DA终端吸收DA减少所致。这项研究的目的之一是调查DA转运蛋白（DAT）在MeHg诱导的DA释放中的作用。 400 microM MeHg和诺米芬（50 microM）或苯丙胺（50 microM）的共输注产生的DA释放增加，类似于诺米芬和苯丙胺单独产生的释放。以同样的方式，MeHg诱导的DA释放在无Ca（2+）的条件下或用利血平（10 mg / kg ip ip）或河豚毒素（TTX）预处理后不会减弱，这表明DA的释放与钙和钙离子无关。囊泡贮藏库，以及不受电压敏感钠通道阻塞的影响。因此，为了研究多巴胺能末端的去极化是否能够影响MeHg诱导的DA释放，我们通过透析膜注入了75 mM KCl。我们的结果清楚地表明，由MeHg诱导的KCl诱发的DA释放减少。综上所述，这些结果表明，MeHg通过转运蛋白依赖性，钙依赖性和水泡依赖性机制诱导DA的释放，并减少了KCl引起的DA释放。

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