Li C, Peoples R W, Weight F F
Laboratory of Molecular and Cellular Neurobiology, National Institute on Alcohol Abuse and Alcoholism, National Institutes of Health, Rockville, MD 20852, USA.
Neuroreport. 1996 Sep 2;7(13):2151-4. doi: 10.1097/00001756-199609020-00018.
ATP stimulates nociceptive neurons via an action on ligand-gated ion channels. Since tissue injury and inflammation result in both localized acidosis and release of ATP, we studied the effect of acid pH on ATP-gated ion channels in rat nodose ganglion neurons. Lowering pH dramatically increased membrane depolarization and action potential firing elicited by ATP. ATP-activated current was enhanced by acid pH and suppressed by alkaline pH. A pH of 7.2 produced the half-maximal effect. Acidification increased the apparent affinity of the receptor for ATP, as evidenced by a parallel shift of the ATP concentration-response curve to the left. The observations suggest that the localized acidosis associated with tissue injury may enhance pain perception via an action on ATP-gated ion channels on mammalian sensory neurons.
三磷酸腺苷（ATP）通过作用于配体门控离子通道刺激伤害性神经元。由于组织损伤和炎症会导致局部酸中毒以及ATP释放，我们研究了酸性pH对大鼠结状神经节神经元中ATP门控离子通道的影响。降低pH会显著增加由ATP引起的膜去极化和动作电位发放。ATP激活电流在酸性pH下增强，在碱性pH下受到抑制。pH为7.2时产生半数最大效应。酸化增加了受体对ATP的表观亲和力，ATP浓度-反应曲线向左平行移动证明了这一点。这些观察结果表明，与组织损伤相关的局部酸中毒可能通过作用于哺乳动物感觉神经元上的ATP门控离子通道来增强痛觉。
