Li Yan-Hai, Wang Jue, Zhang Guangjun
The Key Laboratory of Biomedical Information Engineering of Ministry of Education, and Research Center of Rehabilitation Science and Technology, School of Life Science and Technology, Xi'an Jiaotong University, Xi'an 710049, Shaanxi, People's Republic of China.
Chin J Physiol. 2011 Jun 30;54(3):190-5. doi: 10.4077/cjp.2011.amm020.
Activation of N-methyl-D-aspartate receptors (NMDARs) has been implicated in various forms of synaptic plasticity depending on the receptor subtypes involved. However, the contribution of NR2A and NR2B subunits in the induction of long-term depression (LTD) of excitatory postsynaptic currents (EPSCs) in layer II/III pyramidal neurons of the young rat visual cortex remains unclear. The present study used whole-cell patch-clamp recordings in vitro to investigate the role of NR2A- and NR2B-containing NMDARs in the induction of LTD in visual cortical slices from 12- to 15-day old rats. We found that LTD was readily induced in layer II/III pyramidal neurons of the rat visual cortex with 10-min 1-Hz stimulation paired with postsynaptic depolarization. D-APV, a selective NMDAR antagonist, blocked the induction of LTD. Moreover, the selective NR2B-containing NMDAR antagonists (Ro 25-6981 and ifenprodil) also prevented the induction of LTD. However, Zn2+, a voltage-independent NR2A-containing NMDAR antagonist, displayed no influence on the induction of LTD. These results suggest that the induction of LTD in layer II/III pyramidal neurons of the young rat visual cortex is NMDAR-dependent and requires NR2B-containing NMDARs, not NR2A-containing NMDARs.
根据所涉及的受体亚型不同，N-甲基-D-天冬氨酸受体（NMDARs）的激活与多种形式的突触可塑性有关。然而，NR2A和NR2B亚基在幼鼠视觉皮层II/III层锥体神经元兴奋性突触后电流（EPSCs）的长时程抑制（LTD）诱导中的作用仍不清楚。本研究采用体外全细胞膜片钳记录技术，研究含NR2A和NR2B的NMDARs在12至15日龄大鼠视觉皮层切片LTD诱导中的作用。我们发现，在大鼠视觉皮层II/III层锥体神经元中，通过10分钟1赫兹刺激与突触后去极化配对，很容易诱导出LTD。选择性NMDAR拮抗剂D-APV阻断了LTD的诱导。此外，选择性含NR2B的NMDAR拮抗剂（Ro 25-6981和ifenprodil）也阻止了LTD的诱导。然而，电压非依赖性含NR2A的NMDAR拮抗剂Zn2+对LTD的诱导没有影响。这些结果表明，幼鼠视觉皮层II/III层锥体神经元中LTD的诱导是NMDAR依赖性的，并且需要含NR2B的NMDARs，而不是含NR2A的NMDARs。
