Kainate receptor-mediated synaptic transmissions in the adult rodent insular cortex
Kainate receptor-mediated synaptic transmissions in the adult rodent insular cortex
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DOI：
10.1152/jn.00453.2012
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发表时间：
2012-10-01
影响因子：
2.5
通讯作者：
Zhuo, Min
中科院分区：
文献类型：
--
作者：
Koga, Kohei;Sim, Su-Eon;Zhuo, Min
Koga K，Sim SE，Chen T，Wu LJ，Kaang BK，卓M.海人藻酸受体介导的成年啮齿动物岛叶皮质突触传递。神经生理学杂志108：1988-1998,2012。2012年7月11日首次出版；DOI：10.1152/jn.00453.2012。-kainate(KA)受体在中枢神经系统广泛表达，调节兴奋性和抑制性突触传递。KA受体在恐惧记忆、焦虑和疼痛中发挥重要作用。然而，对它们在岛叶皮质(IC)突触传递中的作用知之甚少，IC是味觉、记忆和疼痛的关键区域。利用全细胞膜片钳记录，我们已经证明KA受体对IC各层神经元的快速突触传递起作用。在GABAA受体拮抗剂印防己毒素、N-甲基-D-天冬氨酸受体拮抗剂AP-5和选择性AMPA受体拮抗剂GYKI 53655存在下，KA受体介导的兴奋性突触后电流(KA EPSCs)被揭示。我们发现，在成年小鼠IC的各层中，Ka EPSCs与AMPA/Ka EPSCs的比例为5-10%。在成年大鼠IC中也发现了类似的结果。与AMPA受体介导的EPSCs相比，KA EPSCs的上升时间进程和衰减时间常数明显减慢。200赫兹的高频重复刺激显著促进了KA-EPSC的总和。此外，GluK1或GluK2亚单位的基因缺失部分减少了突触后Ka EPSCs，GluK2基因敲除小鼠暴露于选择性GluK1拮抗剂UBP 302可以显著减少Ka EPSCs。这些数据表明，GluK1和GluK2在IC中都起着功能作用。我们的研究可能为KA受体在IC相关功能中的生理学和病理学提供突触基础。
Koga K, Sim SE, Chen T, Wu LJ, Kaang BK, Zhuo M. Kainate receptor-mediated synaptic transmissions in the adult rodent insular cortex. J Neurophysiol 108: 1988-1998, 2012. First published July 11, 2012; doi: 10.1152/jn.00453.2012.-Kainate (KA) receptors are expressed widely in the central nervous system and regulate both excitatory and inhibitory synaptic transmission. KA receptors play important roles in fear memory, anxiety, and pain. However, little is known about their function in synaptic transmission in the insular cortex (IC), a critical region for taste, memory, and pain. Using whole cell patch-clamp recordings, we have shown that KA receptors contribute to fast synaptic transmission in neurons in all layers of the IC. In the presence of the GABA A receptor antagonist picrotoxin, the NMDA receptor antagonist AP-5, and the selective AMPA receptor antagonist GYKI 53655, KA receptor-mediated excitatory postsynaptic currents (KA EPSCs) were revealed. We found that KA EPSCs are similar to 5-10% of AMPA/KA EPSCs in all layers of the adult mouse IC. Similar results were found in adult rat IC. KA EPSCs had a significantly slower rise time course and decay time constant compared with AMPA receptor-mediated EPSCs. High-frequency repetitive stimulations at 200 Hz significantly facilitated the summation of KA EPSCs. In addition, genetic deletion of GluK1 or GluK2 subunit partially reduced postsynaptic KA EPSCs, and exposure of GluK2 knockout mice to the selective GluK1 antagonist UBP 302 could significantly reduce the KA EPSCs. These data suggest that both GluK1 and GluK2 play functional roles in the IC. Our study may provide the synaptic basis for the physiology and pathology of KA receptors in the IC-related functions.