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Timely regulated sorting from early to late endosomes is required to maintain cerebellar long-term depression

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  • Taegon Kim

    (Korea Institute of Science and Technology (KIST))

  • Yukio Yamamoto

    (Korea Institute of Science and Technology (KIST))

  • Keiko Tanaka-Yamamoto

    (Korea Institute of Science and Technology (KIST))

Abstract

An important feature of long-term synaptic plasticity is the prolonged maintenance of plastic changes in synaptic transmission. The trafficking of AMPA-type glutamate receptors (AMPARs) is involved in the expression of many forms of synaptic plasticity, yet the subsequent events accomplishing the maintenance of plastic changes in synaptic AMPAR numbers are not fully understood. Here, we find that maintenance of cerebellar long-term depression results from a reduction in the number of AMPARs residing within endocytic recycling pathways. We then develop a genetically encoded, photosensitive inhibitor of late endosome sorting and use this to discover that initial maintenance of long-term depression relies on timely regulated late endosome sorting, which exhibits a threshold as well as switch-like behavior. Thus, our results indicate that recycling AMPAR numbers are reduced by a switching machinery of transient late endosome sorting, and that this process enables the transition from basal synaptic transmission to long-term depression maintenance.

Suggested Citation

  • Taegon Kim & Yukio Yamamoto & Keiko Tanaka-Yamamoto, 2017. "Timely regulated sorting from early to late endosomes is required to maintain cerebellar long-term depression," Nature Communications, Nature, vol. 8(1), pages 1-16, December.
    • Handle: RePEc:nat:natcom:v:8:y:2017:i:1:d:10.1038_s41467-017-00518-3
    DOI: 10.1038/s41467-017-00518-3
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    1. Anika Perdok & Zoë P. Van Acker & Céline Vrancx & Ragna Sannerud & Inge Vorsters & Assunta Verrengia & Zsuzsanna Callaerts-Végh & Eline Creemers & Sara Gutiérrez Fernández & Britt D’hauw & Lutgarde Se, 2024. "Altered expression of Presenilin2 impacts endolysosomal homeostasis and synapse function in Alzheimer’s disease-relevant brain circuits," Nature Communications, Nature, vol. 15(1), pages 1-20, December.

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