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A disinhibitory nigra-parafascicular pathway amplifies seizure in temporal lobe epilepsy.
Nature Communications ( IF 14.7 ) Pub Date : 2020-02-17 , DOI: 10.1038/s41467-020-14648-8 Bin Chen 1 , Cenglin Xu 1 , Yi Wang 1, 2 , Wenkai Lin 1 , Ying Wang 1 , Liying Chen 1 , Heming Cheng 1 , Lingyu Xu 1 , Tingting Hu 1 , Junli Zhao 1 , Ping Dong 1 , Yi Guo 2 , Shihong Zhang 1 , Shuang Wang 2 , Yudong Zhou 1 , Weiwei Hu 1 , Shuming Duan 1 , Zhong Chen 1, 2, 3
Nature Communications ( IF 14.7 ) Pub Date : 2020-02-17 , DOI: 10.1038/s41467-020-14648-8 Bin Chen 1 , Cenglin Xu 1 , Yi Wang 1, 2 , Wenkai Lin 1 , Ying Wang 1 , Liying Chen 1 , Heming Cheng 1 , Lingyu Xu 1 , Tingting Hu 1 , Junli Zhao 1 , Ping Dong 1 , Yi Guo 2 , Shihong Zhang 1 , Shuang Wang 2 , Yudong Zhou 1 , Weiwei Hu 1 , Shuming Duan 1 , Zhong Chen 1, 2, 3
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The precise circuit of the substantia nigra pars reticulata (SNr) involved in temporal lobe epilepsy (TLE) is still unclear. Here we found that optogenetic or chemogenetic activation of SNr parvalbumin+ (PV) GABAergic neurons amplifies seizure activities in kindling- and kainic acid-induced TLE models, whereas selective inhibition of these neurons alleviates seizure activities. The severity of seizures is bidirectionally regulated by optogenetic manipulation of SNr PV fibers projecting to the parafascicular nucleus (PF). Electrophysiology combined with rabies virus-assisted circuit mapping shows that SNr PV neurons directly project to and functionally inhibit posterior PF GABAergic neurons. Activity of these neurons also regulates seizure activity. Collectively, our results reveal that a long-range SNr-PF disinhibitory circuit participates in regulating seizure in TLE and inactivation of this circuit can alleviate severity of epileptic seizures. These findings provide a better understanding of pathological changes from a circuit perspective and suggest a possibility to precisely control epilepsy.
中文翻译：
抑制性黑素-束旁通路增加了颞叶癫痫的发作。
尚不明确参与颞叶癫痫（TLE）的黑质网状组织（SNr）的精确回路。在这里，我们发现SNr小白蛋白+（PV）GABA能神经元的光遗传或化学遗传激活在点燃和卡因酸诱导的TLE模型中放大了癫痫发作的活动，而对这些神经元的选择性抑制则减轻了癫痫发作的活动。癫痫发作的严重程度通过投射到束旁核（PF）的SNr PV纤维的光遗传学操纵来双向调节。电生理学结合狂犬病病毒辅助电路图显示，SNr PV神经元直接投射到功能性抑制后PF GABA能神经元。这些神经元的活动也调节癫痫发作的活动。总的来说，我们的结果表明，远程SNr-PF抑制电路参与了TLE癫痫发作的调节，而该电路的失活可以减轻癫痫发作的严重性。这些发现从回路的角度提供了对病理变化的更好理解，并提出了精确控制癫痫的可能性。
更新日期：2020-02-17
中文翻译：
抑制性黑素-束旁通路增加了颞叶癫痫的发作。
尚不明确参与颞叶癫痫（TLE）的黑质网状组织（SNr）的精确回路。在这里，我们发现SNr小白蛋白+（PV）GABA能神经元的光遗传或化学遗传激活在点燃和卡因酸诱导的TLE模型中放大了癫痫发作的活动，而对这些神经元的选择性抑制则减轻了癫痫发作的活动。癫痫发作的严重程度通过投射到束旁核（PF）的SNr PV纤维的光遗传学操纵来双向调节。电生理学结合狂犬病病毒辅助电路图显示，SNr PV神经元直接投射到功能性抑制后PF GABA能神经元。这些神经元的活动也调节癫痫发作的活动。总的来说，我们的结果表明，远程SNr-PF抑制电路参与了TLE癫痫发作的调节，而该电路的失活可以减轻癫痫发作的严重性。这些发现从回路的角度提供了对病理变化的更好理解，并提出了精确控制癫痫的可能性。
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