Erdélyi L, Such G
Comp Biochem Physiol C Comp Pharmacol Toxicol. 1986;85(2):319-27. doi: 10.1016/0742-8413(86)90201-x.
The effects of capsaicin (CAP) on membrane ionic currents of identified and non-identified neurons were investigated by use of the single electrode clamp (SEC). CAP (300 microM, 22 degrees C, pH 7.4) caused a 25-50% reduction of the inward current and a 50-80% reduction of the outward current in normal or Na-free (Tris) solution. The Na current (INa) was moderately decreased (about 10%) in LPa2 neuron, but a 50% reduction of the peak Ca current (ICa) was observed. The action of CAP on ICa varied from cell to cell but an enhanced inactivation of the fast calcium current was found in all neurons studied. CAP (150 microM, 10 min) highly attenuated the long-lasting component of the inward current in LPa2 recorded in Na-free (TEA) Ba solutions. CAP attenuated the fast outward current (IA) and voltage-dependent outward current (IK) in 100 and 300 microM concentrations for the half blocking dose (ID50) in LPa2 neuron, respectively. CAP decreased the slow outward tail currents but hardly influenced the leakage current (IL). We suggest that the acute action of CAP coupled with a series of events in the neuronal membrane can modify the conductance via electrically excitable calcium, potassium and sodium channels differentially.
采用单电极钳(SEC)研究了辣椒素(CAP)对已识别和未识别神经元膜离子电流的影响。在正常或无钠(Tris)溶液中,CAP(300 microM,22℃,pH 7.4)使内向电流降低25 - 50%,外向电流降低50 - 80%。在LPa2神经元中,钠电流(INa)适度降低(约10%),但观察到峰值钙电流(ICa)降低了50%。CAP对ICa的作用因细胞而异,但在所研究的所有神经元中均发现快速钙电流的失活增强。CAP(150 microM,10分钟)高度减弱了在无钠(TEA)钡溶液中记录的LPa2内向电流的持续成分。在LPa2神经元中,CAP分别以100 microM和300 microM的浓度减弱快速外向电流(IA)和电压依赖性外向电流(IK),其半数阻断剂量(ID50)。CAP降低了缓慢的外向尾电流,但几乎不影响漏电流(IL)。我们认为,CAP的急性作用与神经元膜中的一系列事件相结合,可以通过电兴奋性钙、钾和钠通道差异地改变电导。