Sah P
Neuroscience Group, Faculty of Medicine and Health Sciences, University of Newcastle, Australia.
Proc Biol Sci. 1995 Apr 22;260(1357):105-11. doi: 10.1098/rspb.1995.0066.
Whole-cell and sharp microelectrode recordings were obtained from neurons of rat dorsal motor nucleus of the vagus (DMV) in transverse slices of the rat medulla maintained in vitro. Calcium currents were studied with sodium currents blocked with tetrodotoxin, potassium currents blocked by perfusing the cell with caesium as the main cation and using barium as the charge carrier. From a holding potential of -60 mV, inward currents activated at potentials positive of -50 mV and peaked around 0 mV. Voltage clamping the neuron at more hyperpolarised potentials did not reveal any low-threshold inward current. The inward current was effectively blocked by cadmium (100 microM) and nicked (1 mM), suggesting that it is carried by voltage-dependent calcium channels. The inward current could be separated into three pharmacologically distinct components: 40% of the whole cell current was omega-conotoxin sensitive; 20% of the current was nifedipine sensitive; and the rest was blocked by high concentrations of cadmium and nickel. This remaining current cannot be due to P-type calcium channels as omega-agatoxin had no effect on the inward current. Nifedipine had no significant effect on the action potential. Application of omega-conotoxin reduced the calcium component of the action potential and significantly reduced the potassium current underlying the afterhyperpolarization. Application of charybdotoxin slowed action potential repolarization. When N-type calcium channels were blocked with omega-conotoxin, charybdotoxin was still effective in slowing repolarization. In contrast, charybdotoxin was ineffective ineffective when calcium influx was blocked with the non-specific calcium channel blocker cadmium.(ABSTRACT TRUNCATED AT 250 WORDS)
在体外维持的大鼠延髓横切片中，从大鼠迷走神经背运动核（DMV）的神经元获取全细胞和尖锐微电极记录。使用河豚毒素阻断钠电流、以铯作为主要阳离子灌注细胞并使用钡作为电荷载体来阻断钾电流，从而研究钙电流。从 -60 mV 的 holding 电位开始，内向电流在 -50 mV 以上的电位激活，并在 0 mV 左右达到峰值。将神经元钳制在更超极化的电位时未发现任何低阈值内向电流。内向电流被镉（100 microM）和镍（1 mM）有效阻断，表明它由电压依赖性钙通道携带。内向电流可分为三个药理学上不同的成分：全细胞电流的 40% 对 ω-芋螺毒素敏感；20% 的电流对硝苯地平敏感；其余部分被高浓度的镉和镍阻断。由于 ω-阿加毒素对内向电流没有影响，所以这剩余的电流不可能是由 P 型钙通道引起的。硝苯地平对动作电位没有显著影响。应用 ω-芋螺毒素可降低动作电位的钙成分，并显著降低超极化后电位所依赖的钾电流。应用蝎毒素可减缓动作电位复极化。当用 ω-芋螺毒素阻断 N 型钙通道时，蝎毒素在减缓复极化方面仍然有效。相比之下，当用非特异性钙通道阻滞剂镉阻断钙内流时，蝎毒素则无效。（摘要截断于 250 字）
