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“TOR”-ing Down the Dentate Gate in Temporal Lobe Epilepsy

机译：在颞叶癫痫病的“门”下“ TOR”

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Finally, proving that pathological abnormalities in DG granule cells are sufficient to cause epilepsy does not prove that these abnormalities are necessarily involved in temporal lobe epilepsy, especially in other models or the human condition. More targeted future approaches—selectively reversing specific aspects of DG granule cell dysfunction—will be needed to determine whether and which of these abnormalities are truly necessary for epileptogenesis in this and other models. Similarly, with regard to the involvement of the mTORC1 pathway in epileptogenesis, this and other recent studies provide strong evidence that mTORC1 hyperactivation is sufficient to cause epilepsy (7,8), but further work is needed to determine the conditions under which abnormal mTORC1 activity is necessary for epileptogenesis in acquired temporal lobe epilepsy. mTORC1 may have numerous downstream effects relevant to epileptogenesis and has been implicated in a variety of different models of epilepsy (4). Although in the present study, mTORC1 activation was used primarily as a tool for triggering epileptogenesis and DG granule cell dysfunction, the mechanistic link between mTORC1 and morphological properties of neurons, such as DG granule cells, may be critical for other types of epilepsy beyond the classic mesial temporal lobe epilepsy.
机译：最后，证明DG颗粒细胞的病理异常足以引起癫痫并不能证明这些异常必然与颞叶癫痫有关，尤其是在其他模型或人类疾病中。需要有针对性的未来方法（选择性逆转DG颗粒细胞功能障碍的特定方面）来确定在此模型和其他模型中对于癫痫发生是否真正需要这些异常以及其中哪些异常是真正必要的。同样，关于mTORC1途径参与癫痫发生的研究，这项研究和其他最新研究提供了有力的证据，证明mTORC1过度活化足以引起癫痫（7,8），但是还需要进一步的工作来确定mTORC1异常活动的条件。是获得性颞叶癫痫中癫痫发生所必需的。 mTORC1可能具有与癫痫发生有关的许多下游效应，并已牵涉到多种不同的癫痫模型中（4）。尽管在本研究中，mTORC1激活主要用作触发癫痫发生和DG颗粒细胞功能障碍的工具，但mTORC1与神经元形态特征（如DG颗粒细胞）之间的机制联系对于除癫痫发作以外的其他类型的癫痫病可能至关重要经典的颞中叶癫痫病。

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