在4-阿米诺皮里丁模型中,神经元驱动性细胞生成:去极化阻断和积累启动了类似发作的活动
Elena Yu Proskurina1, Julia L Ergina1, Aleksey V Zaitsev1
1Laboratory of Molecular Mechanisms of Neural Interactions, Sechenov Institute of Evolutionary Physiology and Biochemistry of RAS, 194223 Saint Petersburg, Russia.
快速升的内部神经元通过进入脱极化块来发作,触发金字塔细胞发射和随后的阴道放电. 抑制性神经元中的这种功能障碍是发作发作的关键.
科学领域:
- 神经科学是一个神经科学.
- 的研究研究.
- 细胞电生理学 细胞电生理学
背景情况:
- 驱动发作开始的精确机制尚未完全理解.
- 抑制性内部神经元在发作产生中的作用呈现出一种悖论.
- 快速升的内部神经元对大脑功能至关重要,但与有关.
研究的目的:
- 为了阐明快速升的内部神经元在ictal放电启动中的作用.
- 为了确定导致发作的事件序列.
- 调查发作机制的区域特异性差异.
主要方法:
- 内部神经元和金字塔神经元的同时全细胞记录.
- 超细胞 ([K+]o) 监测在小鼠内腔皮层-海马切片中.
- 利用4-阿米诺皮里丁模型诱导型活动.
主要成果:
- 在进入脱极化块 (DB) 之前,内神经元表现出高频发射.
- DB的发病与细胞外积累的峰值率相关.
- 在内部神经元DB之后,金字塔细胞同步发射,启动ictal放电.
- 脑内皮层神经元在ictal事件期间同步发射,与海马CA1神经元不同.
结论:
- 内部神经元脱极化阻断作为一个时间开关来进行生殖.
- 消抑制和介导的脱极化触发了同步的金字塔神经元活动.
- 快速升的内部神经元功能障碍是焦点的潜在治疗标.
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