首页> 外文期刊>Advances in Experimental Medicine and Biology >Rising taurine and ethanol concentrations in nucleus accumbens interact to produce the dopamine-activating effects of alcohol.
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Rising taurine and ethanol concentrations in nucleus accumbens interact to produce the dopamine-activating effects of alcohol.

机译:牛磺酸的鼻腔和乙醇浓度上升与产生多巴胺激活的醇的活化作用。

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摘要

Alcohol misuse and addiction is a worldwide problem causing enormous individual suffering as well as financial costs for the society. To develop pharmacological means to reduce suffering, we need to understand the mechanisms underlying the effects of ethanol in the brain. Ethanol is known to increase extracellular levels of both dopamine and taurine in the nucleus accumbens (nAc), a part of the brain reward system, but the two events have not been connected. In previous studies we have demonstrated that glycine receptors in the nAc are involved in modulating both basal- and ethanol-induced dopamine output in the same brain region. By means of in vivo microdialysis in freely moving rats we here demonstrate that the endogenous glycine receptor ligand taurine mimics ethanol in activating the brain reward system. Furthermore, administration of systemic ethanol diluted in an isotonic (0.9% NaCl) or hypertonic (3.6% NaCl) saline solution was investigated with respect to extracellular levels of taurine and dopamine in the nAc. We found that ethanol given in a hypertonic solution, contrary to an isotonic solution, failed to increase concentrations of both taurine and dopamine in the nAc. However, a modest, non-dopamine elevating concentration of taurine in the nAc disclosed a dopamine elevating effect of systemic ethanol also when given in a hypertonic solution. We conclude that the elevations of taurine and dopamine in the nAc are closely related and that in order for ethanol to induce dopamine release, a simultaneous increase of extracellular taurine levels in the nAc is required. These data also -provide support for the notion that the nAc is the primary target for ethanol in its dopamine-activating effect after systemic administration and that taurine is a prominent participant in activating the brain reward system.
机译:酒精滥用和成瘾是一个全球问题,导致巨大的个人痛苦以及社会的财务成本。开发药理学手段来减少痛苦,我们需要了解乙醇在大脑中依据的机制。已知乙醇可以增加细胞核和牛磺酸的细胞内水平,在核心尿嘧啶(NAC)中,是大脑奖励系统的一部分,但这两个事件尚未连接。在先前的研究中,我们已经证明NAC中的甘氨酸受体参与调节基础和乙醇诱导的同一脑区的多巴胺产量。通过在自由移动大鼠中的体内微透析,我们在这里证明了内源性甘氨酸受体配体牛磺酸乙醇激活脑奖励系统。此外,在NAC中的牛磺酸和多巴胺的细胞外水平研究了在等渗(0.9%NaCl)或高渗(3.6%NaCl)盐溶液中稀释的全身乙醇。我们发现,在高渗溶液中给出的乙醇,与等渗溶液相反,未能在NAC中增加牛磺酸和多巴胺的浓度。然而,NAC中牛磺酸的适度,非多巴胺升高浓度公开了在高渗溶液中给出的全身乙醇的多巴胺升高效果。我们得出结论,NAC中牛磺酸和多巴胺的升高与乙醇诱导多巴胺释放,需要同时增加NAC的细胞外牛磺酸水平。这些数据也 - 对NAC在全身施用之后,NAC在其多巴胺激活效果中的乙醇是乙醇的主要靶标的载体的支持,并且牛磺酸是激活大脑奖励系统的突出参与者。

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    Institute of Neuroscience and Physiology The Sahlgrenska Academy at University of Gothenburg;

    Institute of Neuroscience and Physiology The Sahlgrenska Academy at University of Gothenburg;

    Institute of Neuroscience and Physiology The Sahlgrenska Academy at University of Gothenburg;

    Institute of Neuroscience and Physiology The Sahlgrenska Academy at University of Gothenburg;

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  • 正文语种 eng
  • 中图分类 基础医学;
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