持续的体内体验触发了新皮质中的突触转塑性
Roger L Clem1, Tansu Celikel, Alison L Barth
1Department of Biological Sciences and Center for the Neural Basis of Cognition, Carnegie Mellon University, Pittsburgh, PA 15213, USA.
概括
持续的感官体验最初会阻碍,然后在老鼠大脑皮层促进突触强化. 这表明了一个动态机制,持续的经验会随着时间的推移改进神经表征.
科学领域:
- 神经科学是一个神经科学.
- 突触性可塑性 突触性可塑性
- 感官处理 感官处理
背景情况:
- 在体内体验可以损害长期增强 (LTP) 和增强长期抑郁 (LTD).
- 这表明,持续的经验可能会降低神经表征,与学习原则相矛盾.
研究的目的:
- 为了研究持续的胡须刺激如何影响老鼠皮层中的突触强化.
- 阐明体验依赖的突触可塑性背后的分子机制.
主要方法:
- 电生理学记录 in vivo 和 in vitro 在小鼠皮层.
- 在持续的感官刺激期间,检查了4-2/3层突触的突触反应.
- 研究了N-甲基-d-亚斯巴达酸 (NMDA) 和甲基酸盐受体 (mGluRs) 的作用.
主要成果:
- 对于最初的突触强化,NMDA受体的激活是必要的,但后来抑制了进一步的强化.
- 持续的感官活动诱导了进一步的突触强化.
- 这种后来的强化需要转基因类谷氨酸受体的激活,而不是NMDA受体.
结论:
- 在持续的感官输入过程中,突触可塑性表现出机制的切换.
- 在初始的NMDA受体依赖强化后,代代酸盐受体会调解体验依赖的突触强化.
- 这为持续经验如何随着时间的推移增强神经表征提供了一个机制.
相关概念视频
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