Bickler P E, Gallego S M
Department of Anesthesia, University of California at San Francisco 94143-0542.
Am J Physiol. 1993 Aug;265(2 Pt 2):R277-81. doi: 10.1152/ajpregu.1993.265.2.R277.
Recent studies suggest that turtles avoid disturbances in brain ionic regulation during anoxia by reducing the activity of brain calcium and sodium channels. Because glutamate released during anoxia may cause cytotoxic elevations in intracellular calcium, blockade of glutamate-mediated calcium channels may be essential for cellular survival. Elevations in intracellular calcium, measured with the fluorescent dye fura 2, were used to assay glutamate-induced activation of calcium channels in cerebrocortical brain slices from rats and turtles. Fourteen hours of anoxia produced long-lasting reduction in glutamate-mediated calcium flux in the turtle brain. Furthermore, a plasma protein from turtles maintained under anoxic conditions produced blockade of glutamate-mediated calcium flux in cortical brain slices from both turtles and rats. These results suggest that long-lasting modulation of brain calcium channels as well as blockade of calcium channel activity by regulatory proteins may play important roles in reducing transcellular ion fluxes in turtles during anoxia.
最近的研究表明,海龟在缺氧期间通过降低脑钙通道和钠通道的活性来避免脑离子调节的紊乱。由于缺氧期间释放的谷氨酸可能导致细胞内钙的细胞毒性升高,因此阻断谷氨酸介导的钙通道对于细胞存活可能至关重要。用荧光染料fura 2测量细胞内钙的升高,以检测谷氨酸诱导的大鼠和海龟大脑皮质脑片中钙通道的激活。14小时的缺氧导致海龟脑中谷氨酸介导的钙通量长期降低。此外,在缺氧条件下饲养的海龟的一种血浆蛋白在海龟和大鼠的皮质脑片中均产生了对谷氨酸介导的钙通量的阻断。这些结果表明,脑钙通道的长期调节以及调节蛋白对钙通道活性的阻断可能在缺氧期间减少海龟跨细胞离子通量方面发挥重要作用。