Department of Neurology, Baylor College of Medicine, Houston, TX 77030, USA.
Neurosci Lett. 2012 Mar 5;511(1):12-7. doi: 10.1016/j.neulet.2012.01.003. Epub 2012 Jan 11.
The calcium control hypothesis posits that postsynaptic calcium increases are required to trigger synaptic plasticity, with large increases inducing LTP and small increases inducing LTD. In CA1 of the hippocampus, however, LTD induced by chemical activation of metabotropic glutamate receptors (agonist-LTD) is independent of increases in postsynaptic calcium. Here we tested whether LTD induced by pairing of presynaptic stimulation with postsynaptic depolarization (synaptic-LTD) is similarly calcium-independent. This protocol induced an NMDA-dependent LTP when paired at 0mV, which was converted to mGluR-dependent LTD when paired at -20mV. The LTD was not blocked by calcium chelation, blockers of L- or T-type voltage-dependent calcium channels, or hyperpolarization to -70mV. We conclude that synaptically induced mGluR-dependent LTD, like agonist induced mGluR LTD, does not require calcium influx for its induction.
钙控制假说认为，突触后钙离子的增加是触发突触可塑性所必需的，较大的增加诱导长时程增强（LTP），较小的增加诱导 LTD。然而，在海马 CA1 区，代谢型谷氨酸受体（激动剂-LTD）的化学激活诱导的 LTD 不依赖于突触后钙离子的增加。在这里，我们测试了通过突触前刺激与突触后去极化（突触-LTD）的配对诱导的 LTD 是否类似地不依赖于钙。当配对在 0mV 时，该方案诱导了一种 NMDA 依赖性 LTP，当配对在-20mV 时，该 LTP 转换为 mGluR 依赖性 LTD。LTD 不受钙螯合剂、L 或 T 型电压依赖性钙通道阻断剂或至-70mV 的超极化的阻断。我们得出结论，突触诱导的 mGluR 依赖性 LTD，与激动剂诱导的 mGluR LTD 一样，其诱导不需要钙离子内流。
