Quertemont Etienne, Devitgh Audrey, De Witte Philippe
Biologie du Comportement, Université catholique de Louvain, Place Croix du Sud 1, 1348 Louvain-la-Neuve, Belgium.
Alcohol. 2003 Jan;29(1):11-9. doi: 10.1016/s0741-8329(02)00324-5.
In recent microdialysis studies, increased extracellular concentrations of taurine after high ethanol dose administration were identified in various rat brain regions. The mechanisms by which ethanol caused these increases in extracellular taurine concentration remained unclear but could be related to ethanol-induced cell swelling. The aim of the current study was to investigate whether changes in the body osmotic state modulate the effects of ethanol on brain extracellular taurine concentrations. In several groups of rats, brain hypoosmotic or hyperosmotic states were superimposed on acute ethanol (2.0-g/kg) injections, and extracellular taurine concentrations within the nucleus accumbens were assessed by using an intracerebral microdialysis procedure. A hypoosmotic state was obtained by systemic administration of water while hyperosmotic states were induced by intraperitoneal injections of hypertonic saline solutions (1.8% or 3.6% saline). In isoosmotic conditions, ethanol induced an immediate and significant increase in taurine microdialysate content, confirming results of previous studies. However, the effects of ethanol on taurine concentrations were modulated by osmotic manipulations. Hypoosmotic conditions significantly potentiated ethanol-induced taurine release. In contrast, ethanol-induced increases in extracellular taurine levels were attenuated by 1.8% saline injection and totally prevented by 3.6% saline administration. These results strongly argue in favor of a primary role of osmoregulation in ethanol-induced taurine release. Ethanol-induced cell swelling probably activates volume-sensitive channels, and taurine passively diffuses outside the cells along its concentration gradient.
在最近的微透析研究中，发现在给大鼠高剂量乙醇后，其大脑不同区域细胞外的牛磺酸浓度有所增加。乙醇导致细胞外牛磺酸浓度升高的机制尚不清楚，但可能与乙醇诱导的细胞肿胀有关。本研究的目的是调查机体渗透压状态的变化是否会调节乙醇对大脑细胞外牛磺酸浓度的影响。在几组大鼠中，将大脑低渗或高渗状态叠加于急性注射乙醇（2.0 g/kg）的过程中，并采用脑内微透析程序评估伏隔核内的细胞外牛磺酸浓度。通过全身给予水来获得低渗状态，而通过腹腔注射高渗盐溶液（1.8%或3.6%的盐水）诱导高渗状态。在等渗条件下，乙醇使牛磺酸微透析液含量立即显著增加，这证实了先前研究的结果。然而，乙醇对牛磺酸浓度的影响受到渗透压操作的调节。低渗条件显著增强了乙醇诱导的牛磺酸释放。相反，注射1.8%的盐水减弱了乙醇诱导的细胞外牛磺酸水平的升高，而注射3.6%的盐水则完全阻止了这种升高。这些结果有力地表明渗透调节在乙醇诱导的牛磺酸释放中起主要作用。乙醇诱导的细胞肿胀可能激活了容积敏感通道，牛磺酸沿其浓度梯度被动扩散到细胞外。
