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首页> 外文期刊>The European Journal of Neuroscience >Enhanced synaptic excitation-inhibition ratio in hippocampal interneurons of rats with temporal lobe epilepsy.
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Enhanced synaptic excitation-inhibition ratio in hippocampal interneurons of rats with temporal lobe epilepsy.

机译：颞叶癫痫大鼠海马interneurons突触兴奋抑制比的增强。

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A common feature of all epileptic syndromes is the repetitive occurrence of pathological patterns of synchronous neuronal activity, usually combined with increased neuronal discharge rates. Inhibitory interneurons of the hippocampal formation control both neuronal synchronization as well as the global level of activity and are therefore of crucial importance for epilepsy. Recent evidence suggests that changes in synaptic inhibition during temporal lobe epilepsy are rather specific, resulting from selective death or alteration of interneurons in specific hippocampal layers. Hence, epilepsy-induced changes have to be analysed separately for different types of interneurons. Here, we focused on GABAergic neurons located at the border between stratum radiatum and stratum lacunosum-moleculare of hippocampal area CA1 (SRL interneurons), which are included in feedforward inhibitory circuits. In chronically epileptic rats at 6-8 months after pilocarpine-induced status epilepticus, frequencies of spontaneous andminiature inhibitory postsynaptic currents were reduced, yielding an almost three-fold increase in excitation-inhibition ratio. Consistently, action potential frequency of SRL interneurons was about two-fold enhanced. Morphological alterations of the interneurons indicate that these functional changes were accompanied by remodelling of the local network, probably resulting in a loss of functional inhibitory synapses without conceivable cell death. Our data indicate a strong increase in activity of interneurons in dendritic layers of the chronically epileptic CA1 region. This alteration may enhance feedforward inhibition and rhythmogenesis and - together with specific changes in other interneurons - contribute to seizure susceptibility and pathological synchronization.
机译：所有癫痫综合征的共同特征是同步神经元活动的病理模式反复出现，通常与神经元放电速率增加相结合。海马结构的抑制性interneurons控制神经元同步以及活动的整体水平，因此对于癫痫至关重要。最近的证据表明，颞叶癫痫发作期间突触抑制的变化是相当特异性的，这是由于特定海马层中选择性死亡或中间神经元的改变所致。因此，必须针对不同类型的中间神经元分别分析癫痫诱发的变化。在这里，我们集中于位于前馈抑制回路中的位于海马区CA1（SRL interneurons）的放射线层和腔层分子之间的边界处的GABA能神经元。在毛果芸香碱诱发的癫痫持续状态后6-8个月的慢性癫痫大鼠中，自发性和微型抑制性突触后电流的频率降低，兴奋抑制率几乎增加了三倍。一致地，SRL中间神经元的动作电位频率提高了约两倍。中间神经元的形态学改变表明，这些功能性改变伴随着局部网络的重塑，可能导致功能性抑制突触的丧失而没有可能的细胞死亡。我们的数据表明，慢性癫痫CA1区树突层中的神经元活性大大增加。这种改变可能会增强前馈抑制和节律，并且-与其他中间神经元的特定变化-有助于癫痫发作易感性和病理同步。

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