Marsh S J, Stansfeld C E, Brown D A, Davey R, McCarthy D
Department of Pharmacology, School of Pharmacy, University of London, U.K.
Neuroscience. 1987 Oct;23(1):275-89. doi: 10.1016/0306-4522(87)90289-2.
The selective excitant and neurotoxic action of capsaicin on vagal sensory neurons in the rat has been investigated in vitro using three techniques: extracellular recording of compound spike potentials from the whole nerve; intracellular recording from ganglion cells using single-electrode current and voltage clamp; and electron microscopy of the nerve and nodose ganglion. Capsaicin (0.1-10 microM) depolarized vagal sensory C fibres and cell bodies, and produced an increased conductance. The conductance increase appeared to be due to an increased permeability to sodium and calcium, plus a secondary increase in potassium (and perhaps chloride) conductance consequent upon calcium entry. The early entry of calcium seems to be a significant priming event in the neurotoxic process, since dramatic ultrastructural changes take place within a few minutes of capsaicin application, which are minimized by removing extracellular calcium ions. The observations indicate that in sensory C neurons capsaicin opens a conductance of limited specificity and that a resultant large calcium entry is closely involved in the rapid development of cell injury.
从整条神经细胞外记录复合动作电位；使用单电极电流和电压钳从神经节细胞进行细胞内记录；以及对神经和结状神经节进行电子显微镜观察。辣椒素（0.1 - 10微摩尔）使迷走神经感觉C纤维和细胞体去极化，并导致电导增加。电导增加似乎是由于对钠和钙的通透性增加，以及钙进入后钾（可能还有氯）电导的继发性增加。钙的早期进入似乎是神经毒性过程中的一个重要引发事件，因为在应用辣椒素后几分钟内就会发生显著的超微结构变化，而通过去除细胞外钙离子可将这些变化最小化。这些观察结果表明，在感觉C神经元中，辣椒素打开了一种特异性有限的电导，并且由此产生的大量钙内流与细胞损伤的快速发展密切相关。
