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内部神经元的第塔阶段锁定控制了发作易感性

Zoé Christenson Wick¹, Paul A Philipsberg¹, Cassidy Kohler¹

¹Nash Family Department of Neuroscience, Icahn School of Medicine at Mount Sinai; New York, 10029, United States.

bioRxiv : the preprint server for biology

|September 18, 2025

概括

改变抑制性神经元活动的时间 (甲相锁定) 会对发作易感性产生因果影响. 在性小鼠中恢复正常的阶段锁定减少了发作,而在健康小鼠中破坏它增加了发作风险.

科学领域:

神经科学是一个神经科学.
的研究研究.
计算神经科学是一种神经科学.

背景情况:

神经元发射时间对大脑功能至关重要,通过像theta这样的振荡来组织.
甲相锁定,即神经元在特定的甲周期阶段发射神经元,为信息处理创造了窗口.
破坏的甲相锁定与神经系统疾病有关,但由于技术限制,其因果作用尚未被证明.

研究的目的:

开发一个闭环光遗传系统 (PhaSER) 来控制内部神经元甲相锁定.
为了调查抑制性甲相锁定在发作易感性中的因果作用.
为了检查中牙状回形 (DG) 中parvalbumin (PV+) 和somatostatin (SOM+) 内神经元之间的theta阶段锁定的差异.

主要方法:

开发了PhaSER,一种闭环光遗传系统,用于精确控制内部神经元相锁定.
在健康和性小鼠模型中记录了PV+和SOM+内部神经元的Theta相锁定概况.
在发作易感性测试期间,利用Phaser操纵DG内部神经元西塔相锁定.

主要成果:

在GD中,PV+和SOM+内部神经元表现出明显的theta阶段锁定模式.
与健康对照对照相比,性小鼠在整个甲基循环中显示分散的PV+内部神经元活动.
在性小鼠中恢复正常的PV+内部神经元西塔相锁定,降低了发作易感性.
在健康小鼠中,破坏正常的PV+内部神经元西塔相锁定增加了发作易感性.

结论:

提供了第一个因果证据,将抑制性甲相锁定与发作易感性联系起来.
证明精确控制抑制性神经元定时可以调节健康和患者大脑中的网络功能.
突出了作为的治疗策略,达阶段锁定准的潜力.

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