Ethanol-induced, nonexocytotic [3H]dopamine release from rat nucleus accumbens slices.
Ethanol-induced, nonexocytotic [3H]dopamine release from rat nucleus accumbens slices.
复制标题
乙醇诱导的、非胞吐[3H]多巴胺从大鼠伏隔核切片中释放。
DOI：
10.1016/s0741-8329(02)00217-3
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发表时间：
2002
期刊：
影响因子：
--
通讯作者：
Yan,Qing-Shan
中科院分区：
文献类型：
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作者：
Yan,Qing-Shan
本研究旨在探讨是否载体依赖性机制参与乙醇诱导的多巴胺释放在体外。在帕吉林存在的情况下，将大鼠延髓核切片与[3 H]多巴胺孵育，然后灌流。自发的[3 H]多巴胺释放不受河豚毒素的加入或撤回的钙，但与诺米芬辛，多巴胺转运蛋白阻滞剂治疗显着增加。将切片暴露于电场刺激（双极脉冲，2 ms长，20 mA，0.5 Hz，持续4 min）、高钾浓度（30 mM，2 min）或乙醇（25-100 mM，2 min）与[3 H]多巴胺释放增加相关。加入河豚毒素或从灌注介质中撤出钙，观察到电或高钾浓度诱发的[3 H]多巴胺释放的75%或更大的抑制，但乙醇诱导的[3 H]多巴胺释放没有改变。诺米芬辛处理增强电或高钾浓度诱发的[3 H]多巴胺释放，但抑制乙醇对[3 H]多巴胺释放的影响。结果表明，乙醇的影响的机制是不同的基础与电刺激或高钾浓度的去极化的影响，并支持的建议，非胞吐，载体介导的机制可能参与乙醇诱发的多巴胺释放在体外。
This study was designed to investigate whether a carrier-dependent mechanism is involved in ethanol-induced dopamine release in vitro. Rat nucleus accumbens slices were incubated with [3H]dopamine in the presence of pargyline and then superfused. Spontaneous [3H]dopamine release was unaffected by addition of tetrodotoxin or withdrawal of calcium, but was increased significantly with treatment with nomifensine, a dopamine transporter blocker. Exposure of the slices to electrical field stimulation (bipolar pulse, 2-ms long, 20 mA, 0.5 Hz for 4 min), high potassium concentration (30 mM, 2 min), or ethanol (25–100 mM, 2 min) was associated with increased [3H]dopamine release. With addition of tetrodotoxin or withdrawal of calcium from the perfusion medium, a 75% or greater inhibition of electrically or high potassium concentration–evoked [3H]dopamine release was observed, but ethanol-induced [3H]dopamine release was not altered. Treatment with nomifensine potentiated electrically or high potassium concentration–evoked [3H]dopamine release, but inhibited the effects of ethanol on [3H]dopamine release from the nucleus accumbens slices. The results indicate that the mechanism underlying the effects of ethanol is different from that underlying the effects of depolarization with electrical stimulation or high potassium concentration and support the suggestion that a nonexocytotic, carrier-mediated mechanism may be involved in ethanol-evoked dopamine release in vitro.