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Updated: Jun 15, 2025

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在CB1R激活下,通过actomyosin介导抑制突触囊释放

Maureen H McFadden1,2, Michel-Boris Emeritt3, Hao Xu4

  • 1Institut Pasteur, Université Paris Cité, Synapse and Circuit Dynamics Laboratory, CNRS UMR 3571, Paris, France.

Translational psychiatry
|August 21, 2024
PubMed
概括

类型-1大麻素受体 (CB1R) 的激活需要神经元的actomyosin收缩性,以长期保持大脑的可塑性. 抑制非肌肉肌肉蛋白II (NMII) 和ROCK恢复了突触囊泡的释放,揭示了一个新的可塑性机制.

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