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首页> 外文期刊>Epilepsy currents >'TOR'-ing down the dentate gate in temporal lobe epilepsy
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'TOR'-ing down the dentate gate in temporal lobe epilepsy

机译:在颞叶癫痫病中“ TOR”向下进入齿状门

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摘要

The dentate gyms (DG) is thought to serve as a gate regulating the spread of excitatory input from the entorhinal cortex into the hippocampus (1). Breakdown of this gating function in the DG has been hypothesized to promote development of epileptogenesis in temporal lobe epilepsy (1,2). A variety of pathological changes in DG granule cells in animal models and patients with temporal lobe epilepsy may contribute to disrupted DG function, including somatic hypertrophy, formation of basilar dendrites, ectopic granule cells within the hilus, and mossy fiber sprouting (3).These and other cellular and molecular abnormalities within the DG may lead to the formation of aberrant, excitatory circuits that result in temporal lobe epilepsy. However, as previous studies linking DG dysfunction and epileptogenesis have primarily been correlative in nature, direct proof that such DG abnormalities can definitively cause temporal lobe epilepsy has been lacking.
机译:齿科体育馆(DG)被认为是调节兴奋性输入从内嗅皮层到海马的传播的大门(1)。据推测,该门控功能在DG中的分解可促进颞叶癫痫中癫痫发生的发展(1,2)。动物模型和颞叶癫痫患者中DG颗粒细胞的各种病理变化可能会导致DG功能破坏,包括体细胞肥大,基底树突的形成,hilus内异位颗粒细胞以及苔藓纤维萌芽(3)。 DG中的其他细胞和分子异常可能导致异常的兴奋性回路的形成,从而导致颞叶癫痫。然而,由于先前将DG功能障碍与癫痫发生联系起来的研究本质上是主要相关的,因此,尚缺乏直接证据证明此类DG异常可以明确导致颞叶癫痫。

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