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突触型 kainate 受体与 INaP 相互作用,将颞叶癫痫中齿状回颗粒细胞的稀疏放电转变为持续的节律模式。

Synaptic kainate receptors in interplay with INaP shift the sparse firing of dentate granule cells to a sustained rhythmic mode in temporal lobe epilepsy.

机构信息

Inserm Unité 901, Marseille 13009, France.

出版信息

J Neurosci. 2011 Jul 27;31(30):10811-8. doi: 10.1523/JNEUROSCI.0388-11.2011.

DOI:10.1523/JNEUROSCI.0388-11.2011
PMID:21795533
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6623106/
Abstract

Dentate granule cells, at the gate of the hippocampus, use coincidence detection of synaptic inputs to code afferent information under a sparse firing regime. In both human patients and animal models of temporal lobe epilepsy, mossy fibers sprout to form an aberrant glutamatergic network between dentate granule cells. These new synapses operate via long-lasting kainate receptor-mediated events, which are not present in the naive condition. Here, we report that in chronic epileptic rat, aberrant kainate receptors in interplay with the persistent sodium current dramatically expand the temporal window for synaptic integration. This introduces a multiplicative gain change in the input-output operation of dentate granule cells. As a result, their sparse firing is switched to an abnormal sustained and rhythmic mode. We conclude that synaptic kainate receptors dramatically alter the fundamental coding properties of dentate granule cells in temporal lobe epilepsy.

摘要

齿状回颗粒细胞位于海马的门口,它们使用突触输入的巧合检测,在稀疏发射模式下对传入信息进行编码。在颞叶癫痫的人类患者和动物模型中,苔藓纤维发芽形成齿状回颗粒细胞之间异常的谷氨酸能网络。这些新的突触通过长时程的红藻氨酸受体介导的事件起作用,而在未成熟的情况下不存在这些事件。在这里,我们报告在慢性癫痫大鼠中,异常的红藻氨酸受体与持续的钠离子电流相互作用,显著扩大了突触整合的时间窗口。这在齿状回颗粒细胞的输入-输出操作中引入了乘法增益变化。结果,它们的稀疏发射被切换到异常的持续和节律模式。我们得出结论,突触红藻氨酸受体在颞叶癫痫中显著改变了齿状回颗粒细胞的基本编码特性。

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Synaptic kainate receptors in interplay with INaP shift the sparse firing of dentate granule cells to a sustained rhythmic mode in temporal lobe epilepsy.突触型 kainate 受体与 INaP 相互作用,将颞叶癫痫中齿状回颗粒细胞的稀疏放电转变为持续的节律模式。
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