ArticleCell reports2022
MAPK signaling and a mobile scaffold complex regulate AMPA receptor transport to modulate synaptic strength.
Article in Cell reports, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 18 citations in OpenAlex.
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- A classic traditional chinese medicine formula for depression: mechanistic insights from phytochemical constituents and multitarget pathways.Psychopharmacology · 2025Article
- Activity-dependent mitochondrial ROS signaling regulates recruitment of glutamate receptors to synapses.eLife · 2024Article
- A Necessary Role for PKC-2 and TPA-1 in Olfactory Memory and Synaptic AMPAR Trafficking inThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2024Article
- Preliminary study on toxicological mechanism of golden cuttlefish (Sepia esculenta) larvae exposed to cd.BMC genomics · 2023Article
- Glycogen synthase kinase 3β (GSK3β) and presenilin (PS) are key regulators of kinesin-1-mediated cargo motility within axons.Frontiers in cell and developmental biology · 2023Review
- E2F4DN Transgenic Mice: A Tool for the Evaluation of E2F4 as a Therapeutic Target in Neuropathology and Brain Aging.International journal of molecular sciences · 2022Review
- Phosphoregulation of Kinesins Involved in Long-Range Intracellular Transport.Frontiers in cell and developmental biology · 2022Review
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Authors and funding
9 authors at 4 institutions in 1 country.
Funding
Abstract
Synaptic plasticity depends on rapid experience-dependent changes in the number of neurotransmitter receptors. Previously, we demonstrated that motor-mediated transport of AMPA receptors (AMPARs) to and from synapses is a critical determinant of synaptic strength. Here, we describe two convergent signaling pathways that coordinate the loading of synaptic AMPARs onto scaffolds, and scaffolds onto motors, thus providing a mechanism for experience-dependent changes in synaptic strength. We find that an evolutionarily conserved JIP-protein scaffold complex and two classes of mitogen-activated protein kinase (MAPK) proteins mediate AMPAR transport by kinesin-1 motors. Genetic analysis combined with in vivo, real-time imaging in Caenorhabditis elegans revealed that CaMKII is required for loading AMPARs onto the scaffold, and MAPK signaling is required for loading the scaffold complex onto motors. Our data support a model where CaMKII signaling and a MAPK-signaling pathway cooperate to facilitate the rapid exchange of AMPARs required for early stages of synaptic plasticity.
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