Kullmann D M, Perkel D J, Manabe T, Nicoll R A
Department of Pharmacology, University of California, San Francisco 94143-0450.
Neuron. 1992 Dec;9(6):1175-83. doi: 10.1016/0896-6273(92)90075-o.
We have studied the role of Ca2+ entry via voltage-sensitive Ca2+ channels in long-term potentiation (LTP) in the CA1 region of the hippocampus. Repeated depolarizing pulses, in the presence of the NMDA receptor antagonist D-APV and without synaptic stimulation, resulted in a potentiation of excitatory postsynaptic potentials (EPSPs) or currents (EPSCs). This depolarization-induced potentiation was augmented in raised extracellular Ca2+ and was blocked by intracellular BAPTA, a Ca2+ chelator, or by nifedipine, a Ca2+ channel antagonist, indicating that the effect was mediated by Ca2+ entry via voltage-sensitive Ca2+ channels. Although the peak potentiation could be as large as 3-fold, the EPSP(C)s decayed back to baseline values within approximately 30 min. However, synaptic activation paired with depolarizing pulses in the presence of D-APV converted the transient potentiation into a sustained form. These results indicate that a rise in postsynaptic Ca2+ via voltage-sensitive Ca2+ channels can transiently potentiate synaptic transmission, but that another factor associated with synaptic transmission may be required for LTP.
我们研究了通过电压敏感性钙通道进入的钙离子在海马体CA1区长期增强（LTP）中的作用。在NMDA受体拮抗剂D - APV存在且无突触刺激的情况下，重复去极化脉冲导致兴奋性突触后电位（EPSP）或电流（EPSC）增强。这种去极化诱导的增强在细胞外钙离子浓度升高时增强，并被细胞内钙离子螯合剂BAPTA或钙离子通道拮抗剂硝苯地平阻断，表明该效应是由通过电压敏感性钙通道进入的钙离子介导的。尽管峰值增强可达3倍，但EPSP（C）在约30分钟内衰减回基线值。然而，在D - APV存在的情况下，突触激活与去极化脉冲配对可将短暂增强转化为持续形式。这些结果表明，通过电压敏感性钙通道引起的突触后钙离子升高可短暂增强突触传递，但LTP可能需要与突触传递相关的另一个因素。
