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首页> 外文期刊>Addiction biology >Implications for glycine receptors and astrocytes in ethanol-induced elevation of dopamine levels in the nucleus accumbens.
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Implications for glycine receptors and astrocytes in ethanol-induced elevation of dopamine levels in the nucleus accumbens.

机译：甘氨酸受体和星形胶质细胞在乙醇诱导伏隔核中多巴胺水平升高中的意义。

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Elevated dopamine levels are believed to contribute to the rewarding sensation of ethanol (EtOH), and previous research has shown that strychnine-sensitive glycine receptors in the nucleus accumbens (nAc) are involved in regulating dopamine release and in mediating the reinforcing effects of EtOH. Furthermore, the osmoregulator taurine, which is released from astrocytes treated with EtOH, can act as an endogenous ligand for the glycine receptor, and increase extracellular dopamine levels. The aim of this study was to address if EtOH-induced swelling of astrocytes could contribute to elevated dopamine levels by increasing the extracellular concentration of taurine. Cell swelling was estimated by optical sectioning of fluorescently labeled astrocytes in primary cultures from rat, and showed that EtOH (25-150 mM) increased astrocyte cell volumes in a concentration- and ion-dependent manner. The EtOH-induced cell swelling was inhibited in cultures treated with the Na(+) /K(+) /2Cl cotransporter blocker furosemide (1 mM), Na(+) /K(+) -ATPase inhibitor ouabain (0.1 mM), potassium channel inhibitor BaCl (50 microM) and in cultures containing low extracellular sodium concentration (3 mM). In vivo microdialysis performed in the nAc of awake and freely moving rats showed that local treatment with EtOH enhanced the concentrations of dopamine and taurine in the microdialysate, while glycine and beta-alanine levels were not significantly modulated. EtOH-induced dopamine release was antagonized by local treatment with the glycine receptor antagonist strychnine (20 microM) or furosemide (100 microM or 1 mM). Furosemide also prevented EtOH-induced taurine release in the nAc. In conclusion, our data suggest that extracellular concentrations of dopamine and taurine are interconnected and that swelling of astrocytes contributes to the acute rewarding sensation of EtOH.
机译：多巴胺水平升高被认为有助于改善乙醇（EtOH）的感觉，以前的研究表明伏隔核（nAc）中对苯丙氨酸敏感的甘氨酸受体参与调节多巴胺的释放和介导EtOH的增强作用。此外，从用EtOH处理过的星形胶质细胞释放的渗透调节剂牛磺酸可作为甘氨酸受体的内源性配体，并增加细胞外多巴胺水平。这项研究的目的是要解决由EtOH诱导的星形胶质细胞肿胀是否可以通过增加牛磺酸的细胞外浓度来促进多巴胺水平升高。通过对大鼠原代培养物中荧光标记的星形胶质细胞进行光学切片来估计细胞肿胀，结果表明EtOH（25-150 mM）以浓度和离子依赖性方式增加了星形胶质细胞的体积。在用Na（+）/ K（+）/ 2Cl共转运蛋白阻断剂速尿（1 mM），Na（+）/ K（+）-ATPase抑制剂哇巴因（0.1 mM）处理的培养物中，EtOH诱导的细胞肿胀得到抑制钾通道抑制剂BaCl（50 microM）和含有低细胞外钠浓度（3 mM）的培养物中。在清醒和自由移动的大鼠的nAc中进行的体内微透析显示，局部用EtOH处理可提高微透析液中多巴胺和牛磺酸的浓度，而甘氨酸和β-丙氨酸的水平并未受到明显调节。 EtOH诱导的多巴胺释放被甘氨酸受体拮抗剂士的宁（20 microM）或速尿（100 microM或1 mM）局部处理所拮抗。速尿还阻止了nAc中EtOH诱导的牛磺酸释放。总之，我们的数据表明细胞外浓度的多巴胺和牛磺酸是相互联系的，星形胶质细胞的肿胀有助于EtOH的急性增感。

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