Shkryl V M, Nikolaenko L M, Kostyuk P G, Lukyanetz E A
Department of General Physiology of Nervous System, Bogomoletz Institute of Physiology, Bogomoletz str. 4, 252024, Kiev, Ukraine.
Brain Res. 1999 Jul 3;833(2):319-28. doi: 10.1016/s0006-8993(99)01575-9.
Whole-cell patch clamp recordings in combination with direct control and measurements of O2 tension (pO2) in bath solution were used to determine the sensitivity of Ca2+ channels of cultured hippocampal neurones to hypoxia in glucose free solution. In all tested neurones, a lowering of pO2 to 4/50 mmHg did not induce changes either in magnitude, kinetics or voltage-current relations of total Ca2+ currents, which composed mainly from two types, L-type (64%) and N-type (31%) components. Hypoxia only induced a delay of Ca2+ current run-down about 27.5% and 39% at 50 and 4 mmHg pO2 respectively that presumably depended on changes in cytoplasmic channel-modulatory metabolites. The obtained results demonstrate that Ca2+ channel molecules in cultured hippocampal neurones are themselves insensitive to short-lasting (10-20 min) oxygen and glucose deprivation, and that they are not a principal target for hypoxic influences on hippocampal function.
采用全细胞膜片钳记录技术,并结合对浴液中氧张力(pO2)的直接控制和测量,来确定培养的海马神经元的Ca2+通道在无糖溶液中对缺氧的敏感性。在所有测试的神经元中,将pO2降至4/50 mmHg时,总Ca2+电流的幅度、动力学或电压-电流关系均未发生变化,总Ca2+电流主要由两种类型组成,即L型(64%)和N型(31%)成分。缺氧仅分别在50 mmHg和4 mmHg pO2时使Ca2+电流衰减延迟约27.5%和39%,这可能取决于细胞质通道调节代谢物的变化。所得结果表明,培养的海马神经元中的Ca2+通道分子本身对短期(10 - 20分钟)的缺氧和无糖环境不敏感,并且它们不是缺氧影响海马功能的主要靶点。