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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 >Selegiline induces dopamine release through ATP-sensitive potassium channels in the rat caudate-putamen in vitro.
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Selegiline induces dopamine release through ATP-sensitive potassium channels in the rat caudate-putamen in vitro.

机译：司来吉兰在大鼠尾状-丘脑中通过ATP敏感性钾通道诱导多巴胺释放。

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摘要

We used superfusion chambers to investigate the role of ATP-sensitive potassium (KATP) channels in dopamine (DA) release elicited by the monoamine oxidase inhibitor selegiline in the rat caudate-putamen in vitro. Selegiline (R[-]-deprenyl], but not the S[+] enantiomer, concentration-dependently induced increases in extracellular concentrations of DA, with a maximal increase to 185% in comparison to basal outflow at 0.1 mM selegiline. Since in our experimental conditions exclusive MAO inhibition does not lead to an enhancement of extracellular DA levels, the effect of selegiline on DA levels seems not to be related to MAO inhibition. Butanedione (0.1 mM), a specific KATP channel blocker, also significantly enhanced extracellular DA levels in the rat caudate-putamen to approx. 260%. Selegiline only led to an additional increase of DA outflow, when added to submaximal concentrations of butanedione or tolbutamide, implying that selegiline is acting on identical sites. When the KATP channel opener cromakalim was added to the incubation medium, basal as well as butanedione-enhanced DA levels markedly decreased to about 40% when compared to baseline values. Selegiline-activated DA release was also antagonized by cromakalim. The selegiline effect was neither modulated by preincubation with the uptake inhibitor nomifensine nor by the DA agonist quinpirole and antagonist sulpiride. In conclusion these results suggest that selegiline is able to modulate KATP channels in the caudate-putamen of the rat in vitro resulting in an enhancement of striatal DA release.
机译：我们使用灌注室来研究ATP敏感性钾（KATP）通道在大鼠尾状-丘脑中由单胺氧化酶抑制剂司来吉兰引起的多巴胺（DA）释放中的作用。司来吉兰（R [-]-去戊烯基，而不是S [+]对映异构体，浓度依赖性地诱导的DA胞外浓度增加，与0.1 mM司来吉兰的基础流出相比，最大增加到185％。实验条件下，MAO的独家抑制作用不会导致细胞外DA水平的升高，司来吉兰对DA水平的影响似乎与MAO的抑制作用无关;丁二酮（0.1 mM）是一种特殊的KATP通道阻滞剂，也能显着提高细胞外DA的水平在大鼠尾状丘脑中大约有260％的剂量，当将司来吉兰添加到次最大浓度的丁二酮或甲苯磺丁酰胺中时，司来吉兰只会导致DA流出量的增加，这表明司来吉兰作用于相同的部位。与基线值相比，基础液和丁二酮增强的DA水平显着降低至约40％，司来吉兰激活的DA释放也很明显。被克罗马卡林（Cromakalim）困扰。司来吉兰的作用既不通过与摄取抑制剂诺米芬的预温育也不通过DA激动剂喹吡罗和拮抗剂舒必利来调节。总之，这些结果表明司来吉兰能够在体外调节大鼠尾状-丘脑中的KATP通道，从而增加纹状体DA的释放。

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