Department of Physiology, Key Laboratory of Environment and Genes Related to Diseases, Ministry of Education, School of Medicine, Xi'an Jiaotong University, Zhuque Dajie 205, Xi'an, Shaanxi 710061, PR China.
Neuroscience. 2010 Feb 3;165(3):684-91. doi: 10.1016/j.neuroscience.2009.11.030. Epub 2009 Nov 17.
Synaptic depression in the hippocampus at early postnatal stage can be induced by test pulse stimulation (<1 Hz). However, the receptor mechanism for induction of this synaptic depression is unclear. In the present study, we used whole-cell patch clamp recording in vitro to investigate how excitatory and inhibitory synapses onto layer II/III pyramidal neurons of the primary visual cortex adapt to test pulse activation from a previously non-activated (naive) state. We found that excitatory postsynaptic currents (EPSCs) of pyramidal neurons were rapidly depressed by 0.1 Hz stimulation in acutely prepared slices from rats at 11-12 postnatal days, while this phenomena disappeared in slices from young adolescent rats (23-24 postnatal days). By contrast, inhibitory postsynaptic currents (IPSCs) were relatively stable following 0.1 Hz stimulation of rat slices at the same early postnatal stage. Moreover, the test pulse depression of EPSCs was associated with a decrease in 1/coefficient of variation (CV)(2) and no change in the paired-pulse ratio. These data imply silencing of synapses and no significant change either in postsynaptic receptor density or presynaptic terminal release probability. This synaptic depression was unaffected by the competitive NMDA receptor antagonist D-APV. Ca(2+)-permeable AMPA receptor selective antagonists, Naspm or IEM-1460, prevented the induction of the test pulse depression. These data suggest that EPSCs, but not IPSCs, were rapidly depressed by test pulse stimulation in rats at early postnatal stage via a Ca(2+)-permeable AMPA receptor-dependent mechanism.
海马在新生早期的突触抑制可由测试脉冲刺激(<1 Hz)诱导。然而，诱导这种突触抑制的受体机制尚不清楚。在本研究中，我们使用在体全细胞膜片钳记录技术，研究了兴奋性和抑制性突触如何适应来自先前未激活(幼稚)状态的测试脉冲的激活。我们发现，在 11-12 日龄大鼠急性脑片上，0.1 Hz 刺激可迅速使锥体神经元的兴奋性突触后电流(EPSCs)发生去极化，而在 23-24 日龄的幼年大鼠脑片中，这种现象消失。相比之下，在相同的早期新生阶段，0.1 Hz 刺激大鼠脑片时，抑制性突触后电流(IPSCs)相对稳定。此外，EPSCs 的测试脉冲抑制与 1/变异系数(CV)(2)的降低有关，而突触后受体密度或突触前末梢释放概率没有变化。这种突触抑制不受竞争性 NMDA 受体拮抗剂 D-APV 的影响。Ca(2+)通透性 AMPA 受体选择性拮抗剂 Naspm 或 IEM-1460 可阻止测试脉冲抑制的诱导。这些数据表明，在新生早期的大鼠中，通过 Ca(2+)通透性 AMPA 受体依赖性机制，EPSCs 而非 IPSCs 可被测试脉冲刺激迅速抑制。
