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首页> 外文期刊>Addiction biology >Alcohol drinking and deprivation alter basal extracellular glutamate concentrations and clearance in the mesolimbic system of alcohol-preferring (P) rats.
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Alcohol drinking and deprivation alter basal extracellular glutamate concentrations and clearance in the mesolimbic system of alcohol-preferring (P) rats.

机译：饮酒和禁食会改变嗜酒精（P）大鼠的中脑边缘系统的基础细胞外谷氨酸浓度和清除率。

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摘要

The present study determined the effects of voluntary ethanol drinking and deprivation on basal extracellular glutamate concentrations and clearance in the mesolimbic system and tested the hypothesis that chronic ethanol drinking would persistently increase basal glutamate neurotransmission. Three groups of alcohol-preferring (P) rats were used: 'water group (WG),' 'ethanol maintenance group (MG; 24-hour free choice water versus 15% ethanol)' and 'ethanol deprivation group (DG; 2 weeks of deprivation).' Quantitative microdialysis and Western blots were conducted to measure basal extracellular glutamate concentrations, clearance and proteins associated with glutamate clearance. Chronic alcohol drinking produced a 70-100% increase of basal extracellular glutamate concentrations in the posterior ventral tegmental area (4.0 versus 7.0?μM) and nucleus accumbens shell (3.0 versus 6.0?μM). Glutamate clearances were reduced by 30-40% in both regions of MG rats compared with WG rats. In addition, Western blots revealed a 40-45% decrease of excitatory amino transporter 1 (EAAT1) protein, but no significant changes in the levels of EAAT2 or cystine-glutamate antiporter in these regions of MG versus WG rats. The enhanced glutamate concentrations returned to control levels, accompanied by a recovery of glutamate clearance following deprivation. These results indicated that chronic alcohol drinking enhanced extracellular glutamate concentrations in the mesolimbic system, as a result, in part, of reduced clearance, suggesting that enhanced glutamate neurotransmission may contribute to the maintenance of alcohol drinking. However, because the increased glutamate levels returned to normal after deprivation, elevated glutamate neurotransmission may not contribute to the initiation of relapse drinking.
机译：本研究确定了自愿饮酒和禁酒对中脑边缘系统中基础细胞外谷氨酸浓度和清除率的影响，并检验了长期饮酒会持续增加基础谷氨酸神经传递的假设。使用三组偏好酒精的（P）大鼠：“水组（WG）”，“乙醇维持组（MG; 24小时自由选择水与15％乙醇的对比）”和“乙醇剥夺组（DG; 2周）剥夺）。”进行了定量的微透析和蛋白质印迹，以测量基础细胞外谷氨酸的浓度，清除率和与谷氨酸清除率相关的蛋白质。长期饮酒会使后腹盖区（4.0 vs 7.0？μM）和伏隔核壳（3.0 vs 6.0？μM）的基础细胞外谷氨酸浓度增加70-100％。与WG大鼠相比，MG大鼠的两个区域的谷氨酸清除率降低了30-40％。此外，蛋白质印迹显示，与WG大鼠相比，这些区域的兴奋性氨基转运蛋白1（EAAT1）蛋白减少了40-45％，但EAAT2或胱氨酸-谷氨酸逆转运蛋白的水平没有显着变化。增强的谷氨酸盐浓度恢复到对照水平，并伴随着剥夺后谷氨酸盐清除率的恢复。这些结果表明，长期饮酒会增加中脑边缘系统中细胞外谷氨酸的浓度，部分是由于清除率降低，提示谷氨酸的神经传递增强可能有助于维持饮酒。但是，由于剥夺后增加的谷氨酸水平恢复正常，因此谷氨酸神经递质的升高可能无助于复发性饮酒。

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