Kollarik Marian, Undem Bradley J
Johns Hopkins University School of Medicine, Baltimore, MD, USA.
J Physiol. 2002 Sep 1;543(Pt 2):591-600. doi: 10.1113/jphysiol.2002.022848.
The mechanisms underlying the response of airway afferent nerves to low pH were investigated in an isolated guinea-pig airway nerve preparation. Extracellular recordings were made from single jugular or nodose vagal ganglion neurons that projected their sensory fibers into the airways. The airway tissue containing the mechanically sensitive receptive fields was exposed into acidic solutions. Rapid and transient (approximately 3 s) administration of 1 mM citric acid to the receptive field consistently induced action potential discharge in nociceptive C-fibers (41/44) and nodose Adelta fibres (29/30) that are rapidly adapting low threshold mechanosensors (RAR-like fibres). In contrast, citric acid activated only 8/17 high threshold mechanosensitive jugular Adelta fibres. The RAR-like fibres were slightly more sensitive than C-fibres to acidic solutions (pH threshold > 6.7). The RAR-like fibres response to the approximately 3 s acid treatment was not affected by a vanilloid receptor 1 (VR1) antagonist, capsazepine (10 microM), and was rapidly inactivating (action potential discharge terminated before the acid administration was completed). Gradual reduction of pH did not activate the RAR-like fibres even when the pH was reduced to approximately 5.0. The C-fibres responded to the gradual reduction of pH with persistent action potential discharge that was nearly abolished by capsazepine (10 microM) and inhibited by over 70 % with another VR1 antagonist iodo-resiniferatoxin (1 microM). In contrast the C-fibre response to the transient approximately 3 s exposure to pH approximately 5.0 was not affected by the VR1 antagonists. We conclude that activation of guinea-pig airway afferents by low pH is mediated by both slowly and rapidly inactivating mechanisms. We hypothesize that the slowly inactivating mechanism, present in C-fibres but not in RAR-like fibres, is mediated by VR1. The rapidly inactivating mechanism acts independently of VR1, has characteristics similar to acid sensing ion channels (ASICs) and is found in the airway terminals of both C-fibres and RAR-like fibres.
在豚鼠离体气道神经标本中研究了气道传入神经对低pH反应的潜在机制。从单个颈静脉或结状迷走神经节神经元进行细胞外记录,这些神经元将其感觉纤维投射到气道中。将含有机械敏感感受野的气道组织暴露于酸性溶液中。向感受野快速且短暂地(约3秒)施加1 mM柠檬酸,始终能诱导伤害性C纤维(41/44)和结状Aδ纤维(29/30)产生动作电位发放,这些纤维是快速适应的低阈值机械感受器(类RAR纤维)。相比之下,柠檬酸仅激活了17根高阈值机械敏感颈静脉Aδ纤维中的8根。类RAR纤维对酸性溶液的敏感性略高于C纤维(pH阈值>6.7)。类RAR纤维对约3秒酸处理的反应不受香草酸受体1(VR1)拮抗剂辣椒素(10 μM)的影响,且迅速失活(在酸给药完成前动作电位发放终止)。即使pH降至约5.0,pH的逐渐降低也不会激活类RAR纤维。C纤维对pH的逐渐降低以持续的动作电位发放做出反应,该反应几乎被辣椒素(10 μM)消除,并被另一种VR1拮抗剂碘树脂毒素(1 μM)抑制超过70%。相反,C纤维对短暂约3秒暴露于pH约5.0的反应不受VR1拮抗剂的影响。我们得出结论,低pH对豚鼠气道传入神经的激活是由缓慢和快速失活机制介导的。我们假设,存在于C纤维而非类RAR纤维中的缓慢失活机制是由VR1介导的。快速失活机制独立于VR1起作用,具有与酸敏感离子通道(ASICs)相似的特征,且在C纤维和类RAR纤维的气道终末均有发现。