视觉皮层的经验驱动的可塑性受到髓和Nogo受体的限制
Aaron W McGee1, Yupeng Yang, Quentin S Fischer
1Department of Neurology, Yale University School of Medicine, New Haven, CT 06520, USA.
概括
在Nogo-66受体 (NgR) 中的突变破坏了视觉皮层可塑性关键时期的正常关闭. 这导致在缺乏ngr的小鼠中长时间的眼球主导性可塑性,影响神经电路的整合.
科学领域:
- 神经科学是一个神经科学.
- 发育生物学 发展生物学
- 视觉系统研究 视觉系统研究
背景情况:
- 视觉皮层中的眼睛主导地位通常只在关键的发育窗口中发生变化.
- 这种可塑性对于建立正常的视觉处理至关重要.
- 在小鼠中,这种可塑性的停止通常发生在产后20至32天之间.
研究的目的:
- 研究Nogo-66受体 (NgR) 在调节眼主导性可塑性关键期的关闭中的作用.
- 了解ngr信号如何影响经验依赖可塑性后的神经回路的巩固.
主要方法:
- 使用了缺乏Nogo-66受体的淘汰赛小鼠 (NgR-/-小鼠).
- 通过在不同出生后年龄 (青少年,45天,120天) 的单眼剥夺实验评估眼睛主导性可塑性.
- 研究了ngr突变对视觉皮层可塑性的时间和持续时间的影响.
主要成果:
- 在关键期内,ngR-/-小鼠表现出正常的眼球主导性可塑性.
- 然而,在NgR-/-小鼠中,塑性在典型的临界期之后异常持续.
- 在老年NGR-/-小鼠中,眼部主导仍然是塑性,类似于幼年阶段.
结论:
- 通过NgR传递生理信号,涉及诸如Nogo,MAG和OMgp之类的髓衍生因子,对于巩固在可塑性过程中建立的神经回路至关重要.
- 干扰ngr信号传递导致无法停止眼睛主导性可塑性.
- 这些发现表明,ngR在稳定视觉皮层电路方面发挥着关键作用,并可能对理解神经损伤后的恢复产生影响.
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