Synaptic activation of kainate receptors on hippocampal interneurons
Synaptic activation of kainate receptors on hippocampal interneurons
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DOI：
10.1038/2194
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发表时间：
1998-10-01
影响因子：
25
通讯作者：
Nicoll, RA
中科院分区：
文献类型：
--
作者：
Frerking, M;Malenka, RC;Nicoll, RA
虽然已知红藻氨酸受体激活可诱发癫痫样活动，但对红藻氨酸受体在突触传递中的作用知之甚少。在这里，我们报告，红藻氨酸（KA）受体存在于中间神经元，激活时，引起自发的抑制性突触后电流（IPSC）驱动的动作电位的频率大幅增加。兴奋性传入神经的刺激产生由中间神经元中的KA受体介导的可识别的突触电流。这种突触电流在其对短刺激串的响应、电流-电压关系和变异系数方面与AM PA受体介导的突触电流相似，但其峰值幅度小得多，速度慢得多。KA应用也显著抑制诱发的IPSC。这种抑郁症似乎是在很大程度上的间接后果的重复发射诱发的神经元间体细胞/树突状KA受体的激活。
Although kainate receptor activation has been known to evoke epileptiform activity, little is known about the role of kainate receptors in synaptic transmission. Here we report that kainate (KA) receptors are present on interneurons and, when activated, cause a large increase in the frequency of spontaneous inhibitory postsynaptic currents (IPSCs) driven by action potentials. Stimulation of excitatory afferents generates a pharmacologically identifiable synaptic current mediated by KA receptors in interneurons. This synaptic current is similar to that mediated by AM PA receptors in its response to short stimulus trains, current-voltage relations and coefficient of variation, but it is much smaller in peak amplitude and much slower. KA application also considerably depresses evoked IPSCs. This depression seems to be in large part an indirect consequence of the repetitive firing evoked by the activation of the interneuronal somatic/dendritic KA receptors.