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首页> 外文期刊>The European Journal of Neuroscience >Background potassium channel block and TRPV1 activation contribute to proton depolarization of sensory neurons from humans with neuropathic pain.
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Background potassium channel block and TRPV1 activation contribute to proton depolarization of sensory neurons from humans with neuropathic pain.

机译：背景钾通道阻滞和TRPV1激活导致患有神经性疼痛的人的感觉神经元质子去极化。

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Abstract Protons cause a sustained depolarization of human dorsal root ganglion (DRG) neurons [Baumann et al. (1996) Pain, 65, 31-38]. In the present study we sought to determine which ion channels are expressed in human DRG neurons that could mediate the sustained responses observed in the patch-clamp recordings. RT-PCR of material from the DRG tissue revealed the presence of mRNAs for a nonselective cation channel that is activated by protons (TRPV1) and background potassium channels that are blocked by protons (TASK-1, TASK-3 and Kir2.3). Highly acidic solution (pH 5.4) applied to cultured DRG neurons evoked prolonged currents that were associated with a net increase in membrane conductance. Consistent with the involvement of TRPV1, these proton-evoked currents were blocked by capsazepine and were only found in neurons that responded to capsaicin with an increase in membrane conductance. Less acidic extracellular solution (pH 6.0) evoked such currents only rarely, but was able to strongly enhance the currents evoked by capsaicin. Capsazepine (1 micro m) blocked the currents evoked by capsaicin at pH 7.35, as well as the potentiated responses to capsaicin at pH 6.0. In neurons that were not excited by capsaicin, moderate extracellular acidification (pH 6.0) caused a sustained decrease in resting membrane conductance. The decrease in membrane conductance by protons was associated with inhibition of background potassium channels. This excitatory effect of protons was not blocked by capsazepine. We conclude that in most neurons the sustained depolarization in response to moderately acidic solutions is the result of blocked background potassium channels. In a subset of neurons, TRPV1 also contributes.
机译：摘要质子导致人背根神经节（DRG）神经元持续去极化[Baumann等。 （1996）Pain，65，31-38]。在本研究中，我们试图确定在人类DRG神经元中表达了哪些离子通道，这些离子通道可以介导在膜片钳记录中观察到的持续反应。来自DRG组织的物质的RT-PCR显示存在被质子（TRPV1）激活的非选择性阳离子通道和被质子阻断的背景钾通道（TASK-1，TASK-3和Kir2.3）的mRNA。应用于培养的DRG神经元的高酸性溶液（pH 5.4）引起延长的电流，这与膜电导的净增加有关。与TRPV1的参与一致，这些质子诱发的电流被辣椒素阻滞，仅在对辣椒素有反应且膜电导增加的神经元中发现。酸性较低的细胞外溶液（pH 6.0）很少引起这样的电流，但是能够强烈增强辣椒素引起的电流。辣椒素（1微米）阻止了辣椒素在pH 7.35时引起的电流，以及在pH 6.0时对辣椒素的增强反应。在辣椒素未激发的神经元中，适度的细胞外酸化（pH 6.0）导致静息膜电导持续降低。质子膜电导的降低与背景钾通道的抑制有关。质子的这种兴奋作用没有被卡萨平所阻断。我们得出结论，在大多数神经元中，对中度酸性溶液的持续去极化是背景钾通道受阻的结果。在神经元的子集中，TRPV1也起作用。

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