Markram H, Segal M
Center for Neuroscience, Weizmann Institute, Rehovot, Israel.
Brain Res. 1991 Feb 1;540(1-2):322-4. doi: 10.1016/0006-8993(91)90529-5.
We examined the effect of elevating intracellular calcium ([Ca2+]i) on responses to iontophoretically applied N-methyl-D-aspartate (NMDA), and quisqualate in CA1 neurons of the hippocampal slice. Topical application of calcimycin (A23187), a calcium ionophore, potentiated responses to NMDA but not to quisqualate. This potentiation was prevented by loading cells with the calcium chelator, BAPTA, suggesting that the action of calcimycin on NMDA receptors was mediated by an elevation of [Ca2+]i in the recorded cell. The potentiation was also recorded in voltage-clamped and in cesium-loaded cells, suggesting that it was not mediated by non-specific changes in voltage or input resistance of the cell that may have resulted from the rise in [Ca2+]i. We propose that intracellular calcium plays a crucial role in regulating the activity of the NMDA subtype of L-glutamate receptor.
我们研究了提高细胞内钙离子浓度（[Ca2+]i）对海马切片CA1神经元中离子电渗法施加的N-甲基-D-天冬氨酸（NMDA）和quisqualate反应的影响。局部应用钙离子载体A23187（钙霉素）增强了对NMDA的反应，但对quisqualate没有影响。用钙螯合剂BAPTA加载细胞可阻止这种增强作用，这表明钙霉素对NMDA受体的作用是由记录细胞中[Ca2+]i的升高介导的。在电压钳制和铯加载的细胞中也记录到了这种增强作用，这表明它不是由[Ca2+]i升高可能导致的细胞电压或输入电阻的非特异性变化介导的。我们提出细胞内钙在调节L-谷氨酸受体NMDA亚型的活性中起关键作用。
