Evidence map›Paper›PMID 38961250›Full record

ArticleCommunications biology2024

Direct and indirect pathways for heterosynaptic interaction underlying developmental synapse elimination in the mouse cerebellum.

Hisako Nakayama, Taisuke Miyazaki, Manabu Abe, Maya Yamazaki, Yoshinobu Kawamura, Myeongjeong Choo, Kohtarou Konno, Shinya Kawata, Naofumi Uesaka, Kouichi Hashimoto and 4 more

Abstract read
In one paragraph

Article in Communications biology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

11 citing papers in PubMed.

  1. Article
  2. mGluR1 signaling is necessary for strengthening winner climbing fiber inputs in the developing mouse cerebellum.Proceedings of the National Academy of Sciences of the United States of America · 2026
    Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Molecular and Anatomical Strengthening of "Winner" Climbing Fiber Synapses in Developing Mouse Purkinje Cells.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2025
    Article
  9. Review
  10. Article
  11. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

14 authors.

Hisako NakayamaDepartment of Neurophysiology, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan.
Taisuke MiyazakiDepartment of Functioning and Disability, Faculty of Health Sciences, Hokkaido University, Sapporo, Japan.
Manabu AbeDepartment of Cellular Neurobiology, Brain Research Institute, Niigata University, Niigata, Japan.
Maya YamazakiDepartment of Cellular Neurobiology, Brain Research Institute, Niigata University, Niigata, Japan.
Yoshinobu KawamuraDepartment of Neurophysiology, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan.
Myeongjeong ChooDepartment of Neurophysiology, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan.
Kohtarou KonnoDepartment of Anatomy, Hokkaido University Graduate School of Medicine, Sapporo, Japan.
Shinya KawataDepartment of Neurophysiology, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan.
Naofumi UesakaDepartment of Neurophysiology, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan.ORCID 0000-0002-9744-944X
Kouichi HashimotoDepartment of Neurophysiology, Graduate School of Biomedical and Health Sciences, Hiroshima University, Hiroshima, Japan.
Mariko MiyataDivision of Neurophysiology, Department of Physiology, School of Medicine, Tokyo Women's Medical University, Tokyo, Japan.
Kenji SakimuraDepartment of Cellular Neurobiology, Brain Research Institute, Niigata University, Niigata, Japan.
Masahiko WatanabeDepartment of Anatomy, Hokkaido University Graduate School of Medicine, Sapporo, Japan.
Masanobu KanoDepartment of Neurophysiology, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan. mkano-tky@m.u-tokyo.ac.jp.ORCID 0000-0002-0725-3292

Funding

MEXT | Japan Society for the Promotion of Science (JSPS) 16H06276MEXT | Japan Society for the Promotion of Science (JSPS) 18H04012MEXT | Japan Society for the Promotion of Science (JSPS) 20H05915MEXT | Japan Society for the Promotion of Science (JSPS) 20H05916MEXT | Japan Society for the Promotion of Science (JSPS) 20K06862MEXT | Japan Society for the Promotion of Science (JSPS) 21H04785
6 · The paper itself

Abstract

Developmental synapse elimination is crucial for shaping mature neural circuits. In the neonatal mouse cerebellum, Purkinje cells (PCs) receive excitatory synaptic inputs from multiple climbing fibers (CFs) and synapses from all but one CF are eliminated by around postnatal day 20. Heterosynaptic interaction between CFs and parallel fibers (PFs), the axons of cerebellar granule cells (GCs) forming excitatory synapses onto PCs and molecular layer interneurons (MLIs), is crucial for CF synapse elimination. However, mechanisms for this heterosynaptic interaction are largely unknown. Here we show that deletion of AMPA-type glutamate receptor functions in GCs impairs CF synapse elimination mediated by metabotropic glutamate receptor 1 (mGlu1) signaling in PCs. Furthermore, CF synapse elimination is impaired by deleting NMDA-type glutamate receptors from MLIs. We propose that PF activity is crucial for CF synapse elimination by directly activating mGlu1 in PCs and indirectly enhancing the inhibition of PCs through activating NMDA receptors in MLIs.

Indexed as

CerebellumReceptors, Metabotropic GlutamateSynapsesAnimalsInterneuronsMiceMice, Inbred C57BLMice, KnockoutPurkinje CellsReceptors, AMPAReceptors, N-Methyl-D-Aspartatemetabotropic glutamate receptor type 1Receptors, AMPAReceptors, Metabotropic GlutamateReceptors, N-Methyl-D-Aspartate

Identifiers

PMID38961250
PMCPMC11222442

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.