首页> 外文期刊>Epilepsy research >Cell type-specific changes in spontaneous and minimally evoked excitatory synaptic activity in hippocampal CA1 interneurons of kainate-treated rats.
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Cell type-specific changes in spontaneous and minimally evoked excitatory synaptic activity in hippocampal CA1 interneurons of kainate-treated rats.

机译:海藻酸盐治疗的大鼠海马CA1中间神经元自发和最小诱发兴奋性突触活动中的细胞类型特异性变化。

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The epileptiform activity in the kainic acid (KA) model of epilepsy arises from complex changes in excitation and inhibition. To assess the involvement of excitatory drive onto inhibitory interneurons in this epileptiform activity, we examined changes in spontaneous and minimally evoked excitatory post-synaptic currents (sEPSCs and eEPSCs) in CA1 interneurons in stratum oriens/alveus (O/A) and stratum radiatum (RAD) in rat hippocampal slices after KA treatment. The frequency and amplitude of sEPSCs and the amplitude of eEPSCs were unchanged in O/A interneurons, but the EPSC kinetics were significantly slower. These changes appear to be due to altered kinetics and voltage-dependent properties of the NMDA component of EPSCs in O/A interneurons. In contrast, sEPSCs and eEPSCs in RAD interneurons did not change after KA treatment. The distinct changes in excitatory synaptic activity in interneurons differentially involved in feedback (O/A) versus feedforward (RAD) inhibition suggest a cell type-specific reorganization of excitatory synapses after KA treatment. These modifications in excitatory input to interneurons could contribute to the maintenance of inhibition of CA1 pyramidal cells after KA treatment, or may also create network conditions favourable to epileptiform activity.
机译:海藻酸(KA)模型的癫痫样活动是由兴奋和抑制的复杂变化引起的。为了评估兴奋性驱动在这种癫痫样活动中对抑制性中枢神经的参与,我们研究了层状天体/肺泡(O / A)和放射状层(CA1)中神经元中自发和最小诱发的突触后电流(sEPSC和eEPSC)的变化。 KA处理后,在大鼠海马切片中添加RAD)。在O / A中间神经元中,sEPSC的频率和幅度以及eEPSC的幅度没有变化,但是EPSC动力学明显变慢。这些变化似乎是由于O / A中间神经元中EPSC的NMDA组分的动力学和电压依赖性特性发生了变化。相反,在KA处理后,RAD中神经元中的sEPSC和eEPSC并未改变。在反馈(O / A)与前馈(RAD)抑制作用不同的中间神经元中,兴奋性突触活性的明显变化表明,KA处理后,细胞类型特异性地重组了兴奋性突触。中间神经元兴奋性输入中的这些修饰可有助于在KA处理后维持对CA1锥体细胞的抑制,或还可创造有利于癫痫样活动的网络条件。

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