Li A, Ségui J, Heinemann S H, Hoshi T
Department of Physiology and Biophysics, Bowen 5660, The University of Iowa, Iowa City, Iowa 52242, USA.
J Neurosci. 1998 Sep 1;18(17):6740-7. doi: 10.1523/JNEUROSCI.18-17-06740.1998.
Functional modifications of neuronal P/Q-type voltage-dependent Ca2+ channels expressed in Xenopus oocytes by oxidation were examined electrophysiologically. Oxidation by external H2O2 enhanced the whole-oocyte currents through the Ca2+ channels composed of the alpha1A, alpha2/delta, and beta3 subunits at negative voltages (<0 mV) without markedly affecting the currents at more positive voltages. Single-channel analysis showed that oxidation accelerates the overall channel opening process. The effect of H2O2 to enhance the Ca2+ channel activity did not require heterologous expression of the alpha2/delta subunit, and it was not mimicked by a cysteine-specific oxidizing agent. The results suggest that oxidative stress may regulate the activity of neuronal Ca2+ channels and that regulation by oxidation may be important in some clinical situations, such as in reperfusion injury after ischemic episodes.
通过电生理学方法研究了氧化作用对非洲爪蟾卵母细胞中表达的神经元P/Q型电压依赖性Ca2+通道的功能修饰。外部H2O2引起的氧化作用增强了在负电压（<0 mV）下通过由α1A、α2/δ和β3亚基组成的Ca2+通道的全卵母细胞电流，而对更正电压下的电流没有明显影响。单通道分析表明，氧化作用加速了通道的整体开放过程。H2O2增强Ca2+通道活性的作用不需要α2/δ亚基的异源表达，且半胱氨酸特异性氧化剂不能模拟该作用。这些结果表明，氧化应激可能调节神经元Ca2+通道的活性，并且氧化调节在某些临床情况中可能很重要，例如缺血发作后的再灌注损伤。
