Morita K, Katayama Y, Koketsu K, Akasu T
Brain Res. 1984 Feb 20;293(2):360-3. doi: 10.1016/0006-8993(84)91243-5.
Adenosine 5'-triphosphate (ATP) produced a long-lasting depolarization in bullfrog spinal ganglion cells. Since the ATP-induced slow depolarization was associated with an increase in membrane resistance and a reverse in polarity (about--90 mV) which was most likely brought about by an inactivation of membrane potassium conductance. In some cells, a rapid and transient depolarization followed by the long-lasting depolarization was produced by ATP and it was markedly reduced in sodium-free solution. ATP reversibly augmented the GABA-induced depolarization which was caused by ionophoresis of GABA. These observations were confirmed using a voltage clamp method. Dose-response analysis of the action of ATP on the GABA-induced response suggests that the facilitatory action of ATP on the GABA response is effected on the GABA receptor channel complexes without changing the GABA affinity.
腺苷 5'-三磷酸（ATP）可使牛蛙脊髓神经节细胞产生持久的去极化。由于 ATP 诱导的缓慢去极化与膜电阻增加以及极性反转（约 -90 mV）相关，这很可能是由于膜钾电导失活所致。在一些细胞中，ATP 可产生快速且短暂的去极化，随后是持久的去极化，并且在无钠溶液中这种去极化明显减弱。ATP 可逆性增强由 GABA 离子电泳引起的 GABA 诱导的去极化。这些观察结果通过电压钳技术得到了证实。对 ATP 对 GABA 诱导反应作用的剂量反应分析表明，ATP 对 GABA 反应的促进作用是在 GABA 受体通道复合物上发挥的，而不改变 GABA 的亲和力。
