Inoue K, Nakazawa K, Fujimori K, Watano T, Takanaka A
Division of Pharmacology, National Institute of Hygienic Sciences, Tokyo, Japan.
Neurosci Lett. 1992 Jan 6;134(2):215-8. doi: 10.1016/0304-3940(92)90520-h.
Characteristics of extracellular ATP-evoked electrical responses in rat hippocampal neurons were investigated. Extracellular ATP (100 microM) induced a rapid depolarization followed by repetitive firings of spikes in these cells under whole-cell current-clamp. In whole-cell voltage-clamp experiments, ATP activated 2 types of inward currents that were inhibited by P2-purinoceptor blocker suramin (300 microM). One is a small (about -20 pA) sustained current which is insensitive to tetrodotoxin (TTX), and the other is a large (-100 to -300 pA) transient current which abolished in the presence of 3 microM TTX. The ATP-induced transient current was blocked by 6-cyano-7-nitro-quinoxaline-2,3-dione (CNQX; 30 microM), a non-N-methyl-D-aspartate (non-NMDA) receptor antagonist. ATP failed to induce the transient current in the cell which showed the desensitization to quisqualic acid (QA; 10 microM), a non-NMDA receptor agonist. These findings suggest that ATP directly activates small sustained currents, and indirectly induces the transient currents by evoking glutamate release.
研究了大鼠海马神经元细胞外ATP诱发的电反应特征。在全细胞膜片钳电流钳模式下，细胞外ATP（100微摩尔）可诱导这些细胞迅速去极化，随后出现重复的锋电位发放。在全细胞膜片钳电压钳实验中，ATP激活了两种内向电流，这两种电流可被P2嘌呤受体阻断剂苏拉明（300微摩尔）抑制。一种是小的（约-20皮安）持续性电流，对河豚毒素（TTX）不敏感，另一种是大的（-100至-300皮安）瞬态电流，在3微摩尔TTX存在时消失。ATP诱导的瞬态电流被非N-甲基-D-天冬氨酸（非NMDA）受体拮抗剂6-氰基-7-硝基喹喔啉-2,3-二酮（CNQX；30微摩尔）阻断。ATP未能在对非NMDA受体激动剂quisqualic acid（QA；10微摩尔）脱敏的细胞中诱导瞬态电流。这些发现表明，ATP直接激活小的持续性电流，并通过诱发谷氨酸释放间接诱导瞬态电流。
