Frerking M, Malenka R C, Nicoll R A
Department of Cellular and Molecular Pharmacology, University of California, San Francisco 94143, USA.
Nat Neurosci. 1998 Oct;1(6):479-86. doi: 10.1038/2194.
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 AMPA 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.
尽管已知海人酸受体激活可诱发癫痫样活动，但对于海人酸受体在突触传递中的作用却知之甚少。在此我们报告，海人酸（KA）受体存在于中间神经元上，并且在被激活时，会导致由动作电位驱动的自发抑制性突触后电流（IPSC）频率大幅增加。刺激兴奋性传入神经会在中间神经元中产生一种可通过药理学鉴定的由KA受体介导的突触电流。这种突触电流在对短刺激串的反应、电流-电压关系和变异系数方面与由AMPA受体介导的突触电流相似，但它的峰值幅度要小得多，且速度要慢得多。应用KA也会显著抑制诱发的IPSC。这种抑制似乎在很大程度上是中间神经元胞体/树突状KA受体激活所诱发的重复放电的间接结果。
