Saransaari P, Oja S S
Tampere Brain Research Center, Medical School, University of Tampere, Tampere, Finland.
Amino Acids. 2006 Jul;31(1):35-43. doi: 10.1007/s00726-006-0290-5. Epub 2006 May 10.
Taurine has been thought to function as a regulator of neuronal activity, neuromodulator and osmoregulator. Moreover, it is essential for the development and survival of neural cells and protects them under cell-damaging conditions. Taurine is also involved in many vital functions regulated by the brain stem, including cardiovascular control and arterial blood pressure. The release of taurine has been studied both in vivo and in vitro in higher brain areas, whereas the mechanisms of release have not been systematically characterized in the brain stem. The properties of release of preloaded [(3)H]taurine were now characterized in slices prepared from the mouse brain stem from developing (7-day-old) and young adult (3-month-old) mice, using a superfusion system. In general, taurine release was found to be similar to that in other brain areas, consisting of both Ca(2+)-dependent and Ca(2+)-independent components. Moreover, the release was mediated by Na(+)-, Cl(-)-dependent transporters operating outwards, as both Na(+)-free and Cl(-) -free conditions greatly enhanced it. Cl(-) channel antagonists and a Cl(-) transport inhibitor reduced the release at both ages, indicating that a part of the release occurs through ion channels. Protein kinases appeared not to be involved in taurine release in the brain stem, since substances affecting the activity of protein kinase C or tyrosine kinase had no significant effects. The release was modulated by cAMP second messenger systems and phospholipases at both ages. Furthermore, the metabotropic glutamate receptor agonists likewise suppressed the K(+)-stimulated release at both ages. In the immature brain stem, the ionotropic glutamate receptor agonists N-methyl-D-aspartate (NMDA) and 2-amino-3-hydroxy-5-methyl-4-isoxazolepropionate (AMPA) potentiated taurine release in a receptor-mediated manner. This could constitute an important mechanism against excitotoxicity, protecting the brain stem under cell-damaging conditions.
牛磺酸一直被认为具有调节神经元活动、神经调质和渗透调节的功能。此外，它对神经细胞的发育和存活至关重要，并在细胞损伤条件下保护它们。牛磺酸还参与脑干调节的许多重要功能，包括心血管控制和动脉血压。牛磺酸的释放已在高等脑区进行了体内和体外研究，而其在脑干中的释放机制尚未得到系统表征。现在，使用灌注系统，对发育中（7日龄）和年轻成年（3月龄）小鼠脑干制备的切片中预加载的[³H]牛磺酸的释放特性进行了表征。一般来说，发现牛磺酸的释放在其他脑区中类似，由钙依赖性和非钙依赖性成分组成。此外，释放是由向外运作的钠依赖性、氯依赖性转运体介导的，因为无钠和无氯条件都极大地增强了它。氯通道拮抗剂和氯转运抑制剂在两个年龄段都降低了释放，表明一部分释放是通过离子通道发生的。蛋白激酶似乎不参与脑干中牛磺酸的释放，因为影响蛋白激酶C或酪氨酸激酶活性的物质没有显著影响。释放受到两个年龄段的环磷酸腺苷第二信使系统和磷脂酶的调节。此外，代谢型谷氨酸受体激动剂在两个年龄段同样抑制钾离子刺激的释放。在未成熟的脑干中，离子型谷氨酸受体激动剂N-甲基-D-天冬氨酸（NMDA）和2-氨基-3-羟基-5-甲基-4-异恶唑丙酸（AMPA）以受体介导的方式增强了牛磺酸的释放。这可能构成一种对抗兴奋性毒性的重要机制，在细胞损伤条件下保护脑干。
