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首页> 美国卫生研究院文献>Frontiers in Psychiatry >A Role for Accumbal Glycine Receptors in Modulation of Dopamine Release by the Glycine Transporter-1 Inhibitor Org25935
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A Role for Accumbal Glycine Receptors in Modulation of Dopamine Release by the Glycine Transporter-1 Inhibitor Org25935

机译：甘氨酸受体在甘氨酸转运蛋白-1抑制剂Org25935对多巴胺释放的调节中的作用。

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Accumbal glycine modulates basal and ethanol-induced dopamine levels in the nucleus accumbens (nAc) as well as voluntary ethanol consumption. Also, systemic administration of the glycine transporter-1 inhibitor elevates dopamine levels in nAc, prevents a further ethanol-induced dopamine elevation and robustly and dose-dependently decreases ethanol consumption in rats. Here we investigated whether applied locally in nAc modulates dopamine release, and whether accumbal glycine receptors or NMDA receptors are involved in this tentative effect. We also addressed whether and ethanol applied locally in nAc interact with dopamine levels, as seen after systemic administration. We used in vivo microdialysis coupled to HPLC-ED in freely moving male Wistar rats to monitor dopamine output in nAc after local perfusion of alone, with ethanol, or -perfusion after pre-treatment with the glycine receptor antagonist strychnine or the NMDA receptor glycine site antagonist L-701.324. Local increased extracellular dopamine levels in a subpopulation of rats. Local strychnine, but not systemic L-701.324, antagonized the dopamine-activating effect of . Ethanol failed to induce a dopamine overflow in the subpopulation responding to with a dopamine elevation. The study supports a role for accumbal glycine receptors rather than NMDA receptor signaling in the dopamine-activating effect of . The results further indicate that the previously reported systemic –ethanol interaction with regard to accumbal dopamine is localized to the nAc. This adds to the growing evidence for the glycine receptor as an important player in the dopamine reward circuitry and in ethanol's effects within this system.
机译：累积甘氨酸调节伏伏核（nAc）中基础和乙醇诱导的多巴胺水平，以及自愿摄入的乙醇。同样，全身性施用甘氨酸转运蛋白-1抑制剂可提高nAc中的多巴胺水平，防止乙醇引起的多巴胺进一步升高，并有力地和剂量依赖性地降低大鼠的乙醇消耗。在这里，我们调查了是否在nAc中局部应用可调节多巴胺的释放，以及是否累积的甘氨酸受体或NMDA受体都参与了这种尝试性作用。正如全身给药后所见，我们还讨论了nAc中局部应用的乙醇是否与多巴胺水平相互作用。我们在自由移动的雄性Wistar大鼠中使用了体内微透析与HPLC-ED联用，以监测在单独使用乙醇局部灌注后或在用甘氨酸受体拮抗剂士的宁或NMDA受体甘氨酸位点预处理后的灌注情况下nAc中多巴胺的输出拮抗剂L-701.324。大鼠亚群中局部增加的细胞外多巴胺水平。局部士的宁，而不是全身性的L-701.324，拮抗了多巴胺的激活作用。乙醇未能在多巴胺升高引起的亚群中诱导多巴胺溢出。这项研究支持了累积型甘氨酸受体而不是NMDA受体信号传导在多巴胺激活作用中的作用。结果进一步表明，先前报道的关于累积多巴胺的全身-乙醇相互作用位于nAc上。这增加了越来越多的证据，证明甘氨酸受体在多巴胺奖赏回路和乙醇在该系统中的作用中起着重要的作用。

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