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首页> 外文期刊>The European Journal of Neuroscience >Alcohol consumption increases basal extracellular glutamate in the nucleus accumbens core of Sprague-Dawley rats without increasing spontaneous glutamate release
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Alcohol consumption increases basal extracellular glutamate in the nucleus accumbens core of Sprague-Dawley rats without increasing spontaneous glutamate release

机译：饮酒会增加Sprague-Dawley大鼠伏隔核核心的基础细胞外谷氨酸，而不会增加自发谷氨酸的释放

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摘要

Glutamate neurotransmission in the nucleus accumbens core (NAc) mediates ethanol consumption. Previous studies using non-contingent and voluntary alcohol administration in inbred rodents have reported increased basal extracellular glutamate levels in the NAc. Here, we assessed basal glutamate levels in the NAc following intermittent alcohol consumption in male Sprague-Dawley rats that had access to ethanol for 7 weeks on alternating days. We found increased basal NAc glutamate at 24 h withdrawal from ethanol and thus sought to identify the source of this glutamate. To do so, we employed a combination of microdialysis, slice electrophysiology and western blotting. Reverse dialysis of the voltage-gated sodium channel blocker tetrodotoxin did not affect glutamate levels in either group. Electrophysiological recordings in slices made after 24 h withdrawal revealed a decrease in spontaneous excitatory postsynaptic current (sEPSC) frequency relative to controls, with no change in sEPSC amplitude. No change in metabotropic glutamate receptor 2/3 (mGlu2/3) function was detected as bath application of the mGlu2/3 agonist LY379268 decreased spontaneous and miniature EPSC frequency in slices from both control and ethanol-consuming rats. The increase in basal glutamate was not associated with changes in the surface expression of GLT-1, however, a decrease in slope of the no-net-flux dialysis function was observed following ethanol consumption, indicating a potential decrease in glutamate reuptake. Taken together, these findings indicate that the increase in basal extracellular glutamate occurring after chronic ethanol consumption is not mediated by an increase in action potential-dependent glutamate release or a failure of mGlu2/3 autoreceptors to regulate such release.
机译：伏伏核（NAc）中谷氨酸的神经传递介导乙醇的消耗。以前在近交啮齿动物中使用非偶然性和自愿性酒精管理的研究报道了NAc中基础细胞外谷氨酸水平的升高。在这里，我们评估了雄性Sprague-Dawley大鼠的间断性饮酒后，NAc中基础谷氨酸的水平，这些大鼠在交替的日子中连续7周接触了乙醇。我们发现从乙醇中撤出24小时后基础NAc谷氨酸含量增加，因此试图确定这种谷氨酸的来源。为此，我们将微透析，切片电生理学和蛋白质印迹相结合。电压门控钠通道阻滞剂河豚毒素的反向透析不影响两组中的谷氨酸水平。停药24小时后在切片中进行的电生理记录显示，自发性兴奋性突触后电流（sEPSC）频率相对于对照组降低，而sEPSC幅度没有变化。没有检测到代谢型谷氨酸受体2/3（mGlu2 / 3）功能的变化，因为在浴液中使用mGlu2 / 3激动剂LY379268可以降低对照组和乙醇摄入大鼠的切片的自发和微型EPSC频率。基底谷氨酸的增加与GLT-1的表面表达的变化无关，但是，乙醇消耗后观察到无净通量透析功能的斜率下降，表明谷氨酸再摄取的潜在减少。综上所述，这些发现表明，慢性乙醇消耗后发生的基础细胞外谷氨酸的增加不是由动作电位依赖性谷氨酸释放的增加或mGlu2 / 3自身受体未能调节这种释放所介导的。

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