长期的强化取决于D-氨酸从星球细胞释放出来
Christian Henneberger1, Thomas Papouin, Stéphane H R Oliet
1UCL Institute of Neurology, University College London, London WC1N 3BG, UK.
Nature
|January 16, 2010
概括
阿斯特罗格利亚释放D-氨酸,使N-甲基-D-酸盐受体 (NMDAR) 依赖的长期增强 (LTP),这是对记忆的关键过程. 这项研究证实,天体细胞衍生的D-素对突触可塑性至关重要.
科学领域:
- 神经科学是一个神经科学.
- 细胞生物学 细胞生物学
- 突触性可塑性 突触性可塑性
背景情况:
- 长期增强 (LTP) 是一种记忆机制模型,传统上依赖于N-甲基-D-酸盐受体 (NMDARs).
- 通过D-氨酸释放调节NMDAR激活的Astroglia的作用已被提出,但由于相互矛盾的实验证据,仍然存在争议.
- 关于质细胞参与LTP的先前研究的生理相关性已受到质疑.
研究的目的:
- 调查星细胞 (Ca2+) 信号在控制依赖NMDAR的LTP的直接作用.
- 为了确定由天体细胞衍生的D-氨酸是否对海马区域的LTP诱导至关重要CA1.1.
主要方法:
- 在单个CA1天体细胞中紧内部Ca2+以观察对附近激发性突触LTP的影响.
- 使用外源D-氨酸或甘氨酸逆转LTP阻塞.
- 在个体星球细胞中降低D-氨酸或破坏外细胞形成,以评估LTP.
- 测量NMDAR协同激剂的部位占用率.
主要成果:
- 在CA1天体细胞中紧内部的Ca2+通过减少NMDAR共激动剂位点占用来阻断附近突触的LTP诱导.
- 这种LTP阻塞是可逆的外源D-或甘氨酸.
- 在单个星球细胞中,D-氨酸的耗尽或异位细胞分裂的破坏也阻断了局部LTP.
结论:
- 星细胞Ca2+依赖D-的释放是控制NMDAR依赖的突触可塑性的关键机制.
- 这种机制调节LTP在星细胞附近的大量激发性突触中.
- 这些发现解决了围绕着细胞参与LTP诱导的争议.
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