Ragozzino D, Eusebi F
Laboratorio Biofisica, Centro Ricerca Sperimentale IRE, Roma, Italy.
Brain Res. 1993 Nov 19;628(1-2):115-20. doi: 10.1016/0006-8993(93)90945-j.
Currents elicited by activation of GABAA, glycine (GLY) and glutamate (GLU) receptors (R) in pyramidal neurons of CA1 region from thin slices of rat hippocampus were studied using the tight-seal whole-cell recording techniques. GLU (100 mM) induced a long-lasting depression of GABA- and GLY-activated currents (IGABA and IGLY) when using standard saline in conjunction with depolarization. The long-lasting depression was not observed: (1) in neurons held at -70 mV during GLU application; (2) in neurons depolarized by current injection but not exposed to GLU; (3) when GLU/depolarization protocol was performed in Ca(2+)-free medium; or (4) by using recording patch-pipettes filled with a medium that tightly controlled cytosolic Ca2+ transients. Sphingosine (10 mM), staurosporine (1 mM) and the specific inhibitor of protein kinase C (PKC(19-36) (200 mM in the patch-pipette solution), blocked the long-lasting depression of IGABA. IGABA was depressed even when the treatment with GLU was performed before patch-clamping the neuron. We conclude that the sustained IGABA and IGLY depression is mediated by cytosolic events triggered by the activation of GLUR.
采用紧密封接全细胞记录技术，研究了大鼠海马薄片CA1区锥体细胞中GABAA、甘氨酸（GLY）和谷氨酸（GLU）受体（R）激活所引发的电流。当使用标准生理盐水并结合去极化时，GLU（100 mM）会诱导GABA和GLY激活电流（IGABA和IGLY）出现长期抑制。在以下情况未观察到这种长期抑制：（1）在施加GLU期间将神经元钳制在-70 mV；（2）通过电流注入使神经元去极化但未暴露于GLU；（3）在无Ca(2+)的培养基中进行GLU/去极化实验方案时；或（4）使用填充有能严格控制胞质Ca2+瞬变的培养基的记录膜片电极时。鞘氨醇（10 mM）、星形孢菌素（1 mM）以及蛋白激酶C（PKC）的特异性抑制剂（膜片电极溶液中为200 mM的PKC(19-36)）可阻断IGABA的长期抑制。即使在对神经元进行膜片钳制之前就用GLU处理，IGABA仍会受到抑制。我们得出结论，IGABA和IGLY的持续抑制是由GLUR激活触发的胞质事件介导的。
