Markram H, Segal M
Center for Neuroscience, Weizmann Institute, Rehovot, Israel.
Neurosci Lett. 1990 May 18;113(1):62-5. doi: 10.1016/0304-3940(90)90495-u.
The effect of acetylcholine (ACh) on intracellular responses to ionophoretic application of N-methyl-D-aspartate (NMDA) was examined in rat hippocampal slice. Recordings were obtained from CA1 neurons under current- and voltage-clamp conditions. Drugs were applied topically by ionophoretic and microdrop techniques. ACh produced an atropine-sensitive potentiation of responses to NMDA. The effect of ACh on NMDA receptor-mediated responses was independent of changes in voltage or potassium conductances caused by ACh. ACh also potentiated responses to L-glutamate but not to kainate or quisqualate. This effect was blocked by DL-2-amino-5-phosphonovalerate (2-APV), an NMDA receptor antagonist. We conclude that ACh, acting on muscarinic receptors, potentiates selectively, the NMDA subclass of L-glutamate receptor.
在大鼠海马切片中，研究了乙酰胆碱（ACh）对离子导入N-甲基-D-天冬氨酸（NMDA）所引起的细胞内反应的影响。在电流钳和电压钳条件下，从CA1神经元进行记录。通过离子导入和微量滴注技术局部应用药物。ACh对NMDA的反应产生了阿托品敏感的增强作用。ACh对NMDA受体介导反应的影响与ACh引起的电压或钾电导变化无关。ACh还增强了对L-谷氨酸的反应，但对海人藻酸或quisqualate没有增强作用。这种作用被NMDA受体拮抗剂DL-2-氨基-5-磷酸戊酸（2-APV）阻断。我们得出结论，作用于毒蕈碱受体的ACh选择性地增强了L-谷氨酸受体的NMDA亚类。
