Halothane enhances acetylcholine release by decreasing dopaminergic activity in rat striatal slices
Halothane enhances acetylcholine release by decreasing dopaminergic activity in rat striatal slices
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DOI：
10.1016/s0197-0186(01)00092-4
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发表时间：
2002-03-01
影响因子：
4.2
通讯作者：
Zsilla, G
中科院分区：
文献类型：
--
作者：
Adachi, YU;Watanabe, K;Zsilla, G
本文研究了氟烷对大鼠纹状体乙酰胆碱（ACh）和多巴胺（DA）释放的影响。氟烷浓度依赖性地抑制DA的释放，而增加ACh的释放。虽然纹状体胆碱能中间神经元的ACh释放受到DA的紧张性调节。氟烷对乙酰胆碱和多巴胺释放关系的影响尚未讨论。利用双标记技术，我们研究了氟烷对乙酰胆碱和多巴胺释放的影响。将切片与[C-14]-胆碱和[H-3]-DA一起孵育，并用含有1 μ M半胆碱-3的改良Krebs溶液灌流。我们施加电场刺激（2 Hz，240次电击），通过从相应刺激期开始时的总流出量中减去基础放射性流出量，计算刺激诱发的放射性释放量。药物对释放的影响表示为刺激诱发的分数释放（FR）的比率，在存在和不存在药物的情况下测量（FRS 2/FRS 1）。氟烷以浓度依赖性方式减少DA释放（在浓度为0、0.5、0.50、0.65、0.671和0.639时，FRS 2/FRS 1 = 0.767 +/-0.021、0.715 +/- 0.026、0.671 +/- 0.014和0.639 +/- 0.033）。2和4%），而乙酰胆碱释放在不同浓度的氟烷的存在下，表现出双相变化。ACh的释放在2%浓度下显著增加，而在0.5%和4%浓度下则无明显增加。氟烷不能增加6-OH-多巴胺损伤后纹状体脑片ACh的释放。苯丙胺的应用减少了ACh的释放，并取消了氟烷的作用，这些结果表明氟烷对ACh释放的影响是间接的：它通过减弱DA释放的抑制作用而增加ACh的释放。氟烷对ACh释放的影响可能与DA和ACh释放之间的非突触相互作用有关。(C)2002爱思唯尔科技有限公司。保留所有权利。
The present study investigated the effect of halothane on acetylcholine (ACh) and dopamine (DA) release from the rat striatum. Halothane decreased DA release in a concentration-dependent manner, while increased ACh release.In our previous investigation, a volatile anesthetic, halothane, inhibited DA release from the rat striatal slices in a concentration-dependent manner. Although the release of ACh from cholinergic interneurons is tonically modulated by DA in the striatum. the effect of halothane on the relationship between the release of ACh and DA has not been discussed. Using double-labeled techniques, we investigated the effect of halothane on ACh and DA release simultaneously. The slices were incubated with [C-14]-choline and [H-3]-DA and superfused with modified Krebs solution containing 1 muM of hemicholinium-3. We applied electrical field stimulation (2 Hz, 240 shocks), and the amount of the release of radioactivity evoked by stimulation was calculated by subtraction of the basal radioactive outflow from the total outflow at the beginning of the respective stimulation periods. The effects of drugs on the release were expressed as the ratio of stimulation-evoked fractional releases (FR), measured in the presence and absence (FRS2/FRS1) of the drug. Halothane decreased DA release in a concentration-dependent manner (FRS2/FRS1 = 0.767 +/- 0.021, 0.715 +/- 0.026, 0.671 +/- 0.014 and 0.639 +/- 0.033 at the concentration of 0, 0.5. 2 and 4%, respectively), while ACh release showed a biphasic change in the presence of different concentrations of halothane. The release of ACh was significantly increased at the concentration of 2%, but not at 0.5 or 4%. Halothane failed to increase the release of ACh in striatal slices after lesion by 6-OH-dopamine. The application of amphetamine reduced the release of ACh and abolished the effect of halothane.These results indicate that the effect of halothane on ACh release is indirect: it increases the release by attenuating the inhibitory effect of DA released from the nigro-striatal pathway. The nonsynaptic interaction between DA and ACh release is involved in the effect of halothane on ACh release. (C) 2002 Elsevier Science Ltd. All rights reserved.