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首页> 外文期刊>Cellular Physiology and Biochemistry >Amino acid osmolytes in regulatory volume decrease and isovolumetric regulation in brain cells: Contribution and mechanisms [Review]
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Amino acid osmolytes in regulatory volume decrease and isovolumetric regulation in brain cells: Contribution and mechanisms [Review]

机译：氨基酸渗透压在脑细胞调节量减少和等容调节中的作用和机制[综述]

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摘要

Brain adaptation to hyposmolarity is accomplished by loss of both electrolytes and organic osmolytes, including amino acids, polyalcohols and methylamines. In brain in vivo, the organic osmolytes account for about 35% of the total solute loss. This review focus on the role of amino acids in cell volume regulation, in conditions of sudden hyposmosis, when cells respond by active regulatory volume decrease (RVD) or after gradual exposure to hyposmotic solutions, a condition where cell volume remains unchanged, named isovolumetric regulation (IVR). The amino acid efflux pathway during RVD is passive and is similar in many respects to the volume-activated anion pathway. The molecular identity of this pathway is still unknown, but the anion exchanger and the phospholemman are good candidates in certain cells. The activation trigger of the osmosensitive amino acid pathway is unclear, but intracellular ionic strength seems to be critically involved. Tyrosine protein kinases markedly influence amino acid efflux during RVD and may play an important role in the transduction signaling cascades for osmosensitive amino acid fluxes. During IVR, amino acids, particularly taurine are promptly released with an efflux threshold markedly lower than that of K+, emphasizing their contribution (possibly as well as of other organic osmolytes) vs inorganic ions, in the osmolarity range corresponding to physiopathological conditions. Amino acid efflux also occurs in response to isosmotic swelling as that associated with ischemia or trauma. Characterization of the pathway involved in this type of swelling is hampered by the fact that most osmolyte amino acids are also neuroactive amino acids and may be released in response to stimuli concurrent with swelling, such as depolarization or intracellular Ca++ elevation. Copyright (C) 2000 S. Karger AG Basel. [References: 76]
机译：脑部对低渗性的适应性通过电解质和有机渗透物（包括氨基酸，多元醇和甲胺）的损失实现。在体内脑中，有机渗透物约占总溶质损失的35％。这篇综述着重于氨基酸在突然低渗状态下的细胞体积调节中的作用，当细胞通过主动调节体积减小（RVD）或逐渐暴露于低渗溶液后，即细胞体积保持不变的状态，称为等容定量调节（IVR）。 RVD期间的氨基酸外排途径是被动的，并且在许多方面与体积激活的阴离子途径相似。该途径的分子身份仍然未知，但是阴离子交换剂和磷酸化lemman在某些细胞中是很好的候选者。渗透敏感的氨基酸途径的激活触发因素尚不清楚，但细胞内离子强度似乎至关重要。酪氨酸蛋白激酶显着影响RVD期间的氨基酸流出，并且可能在渗透敏感氨基酸通量的转导信号级联中起重要作用。在IVR期间，氨基酸，特别是牛磺酸被迅速释放，其流出阈值明显低于K +的阈值，从而强调了它们（相对于无机离子而言）（相对于无机离子而言）在与生理病理条件相对应的渗透压范围内的贡献。氨基酸外流也响应与缺血或创伤相关的等渗肿胀而发生。多数溶菌素氨基酸也是神经活性氨基酸，妨碍了与这种溶胀有关的途径的表征，并且可以响应于与溶胀同时发生的刺激（例如去极化或细胞内Ca ++升高）而释放。版权所有（C）2000 S.Karger AG Basel。 [参考：76]

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