Sauer S K, Weidner C, Carr R W, Averbeck B, Nesnidal U, Reeh P W, Handwerker H O
Department of Physiology and Pathophysiology, University of Erlangen/Nürnberg, Erlangen, Germany.
J Neurophysiol. 2005 Jul;94(1):219-25. doi: 10.1152/jn.00655.2004. Epub 2005 Mar 16.
Threshold tracking of individual polymodal C- and Adelta-fiber terminals was used to assess membrane potential changes induced by de- or hyperpolarizing stimuli in the isolated rat skin-nerve preparation. Constant current pulses were delivered (1 Hz) through a tungsten microelectrode inserted in the receptive field, and the current amplitude was controlled by feedback with a laboratory computer programmed to serially determine the electrical threshold using the method of limits. During threshold tracking, the receptive fields of the fibers were heated (32-46 degrees C in 210 s) or superfused with modified synthetic interstitial fluid containing either 0, 20, 40, 50, or 60 mM [K+], phosphate buffer to pH 5.2 or 6.1, or bradykinin (BK, 10(-8)-10(-5) M). High [K+]e decreased the current threshold for activation by 6-14% over 120 s, whereas K+-free superfusion augmented the threshold by >5%, and after some delay, also induced ongoing discharge in 60% of units. pH 6.1 and 5.2 caused an increase in threshold of 6 and 18%, respectively, and 30% of the fibers were excited by low pH, although the change in threshold of pH responsive and unresponsive fibers did not differ significantly, suggesting a general excitability decrease induced by protons. Heat stimulation increased the mean threshold and conduction velocity of the fibers tested and resulted in activity in 78% of units. Additionally, for these units, activation was preceded by a significant decrease in threshold compared with the tracked thresholds of fibers unresponsive to heat. Bradykinin also led to a significant threshold decrease before activation. In conclusion, the technique of threshold tracking proved suitable to assess changes in excitability resulting from receptor currents evoked by noxious heat and bradykinin in the terminal arborization of cutaneous nociceptors.
采用对单个多模式C纤维和Aδ纤维终末进行阈值跟踪的方法,来评估在离体大鼠皮肤 - 神经标本中,去极化或超极化刺激所诱发的膜电位变化。通过插入感受野的钨微电极施加恒定电流脉冲(1 Hz),电流幅度由实验室计算机通过反馈进行控制,该计算机经编程使用极限法串行确定电阈值。在阈值跟踪过程中,对纤维的感受野进行加热(在210 s内从32℃升至46℃),或用含有0、20、40、50或60 mM [K⁺]、pH值为5.2或6.1的磷酸盐缓冲液的改良合成组织液进行灌流,或用缓激肽(BK,10⁻⁸ - 10⁻⁵ M)进行灌流。高[K⁺]e在120 s内使激活电流阈值降低6 - 14%,而无K⁺灌流使阈值升高>5%,且经过一段时间延迟后,还在60%的单位中诱发持续放电。pH 6.1和5.2分别使阈值升高6%和18%,30%的纤维被低pH值激发,尽管对pH有反应和无反应的纤维阈值变化无显著差异,提示质子诱导普遍的兴奋性降低。热刺激增加了所测试纤维的平均阈值和传导速度,并使78%的单位产生活动。此外,对于这些单位,与对热无反应的纤维的跟踪阈值相比,激活之前阈值有显著降低。缓激肽在激活之前也导致显著的阈值降低。总之,阈值跟踪技术被证明适用于评估皮肤伤害感受器终末分支中,有害热和缓激肽诱发的受体电流所导致的兴奋性变化。