nav18通道抑制毒素与镇痛药物研究进展

tor activity and low-threshold mechanical and acute noxious heat responses but did not respond to noxious mechanical pressure or cold. They also showed a loss of enhanced pain responses and spontaneous pain behavior upon treatment with inflammatory insults. In contrast, nerve injury led to heightened pain sensitivity to thermal and mechanical stimuli indistinguishable from that seen with normal littermates. Pain behavior correlates well with central input from sensory neurons measured electrophysiologically in vivo. These data demonstrate that Nav1.8-expressing neurons are essential for mechanical, cold, and inflammatory pain but not for neuropathic pain or heat sensing.Р删除表达Nav1.8通道的感觉神经元Р图1 应用白喉毒素删除伤害性感受器? (A and B) 用抗外周蛋白(绿色)与抗神经微丝重链抗体(红色)的L4DRG横切面。与对照同胞仔比较(A),在DTA鼠中标记的外周蛋白神经元减少了85%(B)。