Rab10 inactivation promotes AMPAR trafficking and spine enlargement during long-term potentiation

Rab-dependent membrane trafficking is critical for changing the structure and function of dendritic spines during synaptic plasticity. Here, we developed highly sensitive sensors to monitor Rab protein activity in single dendritic spines undergoing structural long-term potentiation (sLTP) in rodent organotypic hippocampal slices. During sLTP, Rab10 was persistently inactivated (>30 min) in the stimulated spines, whereas Rab4 was transiently activated over ~5 min. Inhibiting or deleting Rab10 enhanced sLTP, electrophysiological LTP, and AMPA receptor (AMPAR) trafficking during sLTP. In contrast, disrupting Rab4 impaired sLTP only in the first few minutes and decreased AMPAR trafficking during sLTP. Thus, our results suggest that Rab10 and Rab4 oppositely regulate AMPAR trafficking during sLTP, and inactivation of Rab10 signaling facilitates the induction of LTP and associated spine structural plasticity.

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Published
2024-12-11
DOI
https://doi.org/10.7554/elife.103879
Primary Topic
Neuroscience and Neuropharmacology Research
Type
article
Field-Weighted Citation Impact
0.00

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article

Rab10 inactivation promotes AMPAR trafficking and spine enlargement during long-term potentiation

Paula Parra-Bueno, Timothy E. McGraw, Erzsebet M. Szatmari, Tetsuya Watabe et al.
Neuroscience and Neuropharmacology Research
article

Rab10 inactivation promotes AMPAR trafficking and spine enlargement during long-term potentiation

Paula Parra-Bueno, Timothy E. McGraw, Erzsebet M. Szatmari, Tetsuya Watabe, Goksu Oz, Jun Nishiyama, Elwy Okaz, Ryohei Yasuda, Irena Suponitsky-Kroyter, Jie Wang, Xiaodan Liu
article en

Abstract

Rab-dependent membrane trafficking is critical for changing the structure and function of dendritic spines during synaptic plasticity. Here, we developed highly sensitive sensors to monitor Rab protein activity in single dendritic spines undergoing structural long-term potentiation (sLTP) in rodent organotypic hippocampal slices. During sLTP, Rab10 was persistently inactivated (>30 min) in the stimulated spines, whereas Rab4 was transiently activated over ~5 min. Inhibiting or deleting Rab10 enhanced sLTP, electrophysiological LTP, and AMPA receptor (AMPAR) trafficking during sLTP. In contrast, disrupting Rab4 impaired sLTP only in the first few minutes and decreased AMPAR trafficking during sLTP. Thus, our results suggest that Rab10 and Rab4 oppositely regulate AMPAR trafficking during sLTP, and inactivation of Rab10 signaling facilitates the induction of LTP and associated spine structural plasticity.

Vol. 13
Duke University (US), East Carolina University (US), Hong Kong University of Science and Technology (HK), Cornell University (US), Max Planck Florida Institute for Neuroscience (US), Duke-NUS Medical School (SG), Weill Cornell Medicine (US)
Howard Hughes Medical Institute, National Institutes of Health, Japan Society for the Promotion of Science
Openalex Percentile: Top 76%
Neuroscience and Neuropharmacology Research
DOIOpen Access PDFOpenAlex
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