Huang C S, Song J H, Nagata K, Twombly D, Yeh J Z, Narahashi T
Department of Molecular Pharmacology and Biological Chemistry, Northwestern University Medical School, Chicago, IL 60611, USA.
Brain Res. 1997 Jul 11;762(1-2):235-9. doi: 10.1016/s0006-8993(97)00491-5.
Effects of riluzole on high voltage-activated (HVA) calcium channels of rat dorsal root ganglion neurons were studied using the whole-cell patch-clamp technique. Riluzole at 30 microM inhibited the HVA currents. The onset and offset of riluzole inhibitory effect were slow usually taking more than 3 min. Riluzole inhibition of the HVA currents was abolished and partially reduced by addition of 500 microM GDP-beta-S and 1 mM N-ethylmaleimide, respectively, to the pipette solution. Pre-treatment with pertussis toxin or application of depolarizing pre-pulses did not affect riluzole's inhibitory effect on the HVA currents. Riluzole inhibition of the HVA currents was also blocked by internal application of 50 microg/ml protein kinase A inhibitory peptide. It was concluded that pertussis toxin-insensitive G-proteins and protein kinase A may be involved in riluzole inhibition of the HVA currents.
采用全细胞膜片钳技术研究了利鲁唑对大鼠背根神经节神经元高电压激活（HVA）钙通道的影响。30微摩尔的利鲁唑抑制HVA电流。利鲁唑抑制作用的起始和消退缓慢，通常需要3分钟以上。分别向移液管溶液中加入500微摩尔GDP-β-S和1毫摩尔N-乙基马来酰亚胺后，利鲁唑对HVA电流的抑制作用被消除和部分减弱。用百日咳毒素预处理或施加去极化预脉冲不影响利鲁唑对HVA电流的抑制作用。50微克/毫升蛋白激酶A抑制肽的胞内应用也可阻断利鲁唑对HVA电流的抑制作用。得出的结论是，百日咳毒素不敏感的G蛋白和蛋白激酶A可能参与利鲁唑对HVA电流的抑制作用。
