Evidence map›Paper›PMID 24360545›Full record

ArticleNeuron2013

Kinesin-1 regulates synaptic strength by mediating the delivery, removal, and redistribution of AMPA receptors.

Frédéric J Hoerndli, Dane A Maxfield, Penelope J Brockie, Jerry E Mellem, Erica Jensen, Rui Wang, David M Madsen, Andres V Maricq

Abstract read
In one paragraph

Article in Neuron, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 62 papers.

0numbers the graph read from it
0cells of the map it votes in
62citing 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

62 citing papers in PubMed.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Kinesins inOpen biology · 2025
    Review
  6. Article
  7. Review
  8. Article
  9. Article
  10. Review
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. 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 · 2024
    Article
  17. Article
  18. Article
  19. Review
  20. Article

2 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

8 authors.

Frédéric J HoerndliDepartment of Biology, Center for Cell and Genome Science, University of Utah, Salt Lake City, UT 84112, USA.
Dane A MaxfieldDepartment of Biology, Center for Cell and Genome Science, University of Utah, Salt Lake City, UT 84112, USA.
Penelope J BrockieDepartment of Biology, Center for Cell and Genome Science, University of Utah, Salt Lake City, UT 84112, USA.
Jerry E MellemDepartment of Biology, Center for Cell and Genome Science, University of Utah, Salt Lake City, UT 84112, USA.
Erica JensenDepartment of Biology, Center for Cell and Genome Science, University of Utah, Salt Lake City, UT 84112, USA.
Rui WangDepartment of Biology, Center for Cell and Genome Science, University of Utah, Salt Lake City, UT 84112, USA.
David M MadsenDepartment of Biology, Center for Cell and Genome Science, University of Utah, Salt Lake City, UT 84112, USA.
Andres V MaricqDepartment of Biology, Center for Cell and Genome Science, University of Utah, Salt Lake City, UT 84112, USA. Electronic address: maricq@biology.utah.edu.

Funding

Enhancing and expanding the CGC Strain CollectionP40OD010440 · OD · UNIVERSITY OF MINNESOTA · PI Aric L Daul, Ann E. Rougvie · 2012 to 2026
$7.5M
GLUTAMATE RECEPTOR FUNCTIONR01NS035812 · NINDS · UNIVERSITY OF UTAH · PI MARICQ, ANDRES VILLU · 1997 to 2018
$7.4M
Simultaneous in vivo studies of synapses, neurons, and learning and memoryDP1DA035080 · NIDA · UNIVERSITY OF UTAH · PI MARICQ, ANDRES VILLU · 2012 to 2014
$2.2M
NIDA NIH HHS DP1 DA035080NIH HHS P40 OD010440NINDS NIH HHS NS35812NINDS NIH HHS R01 NS035812
6 · The paper itself

Abstract

A primary determinant of the strength of neurotransmission is the number of AMPA-type glutamate receptors (AMPARs) at synapses. However, we still lack a mechanistic understanding of how the number of synaptic AMPARs is regulated. Here, we show that UNC-116, the C. elegans homolog of vertebrate kinesin-1 heavy chain (KIF5), modifies synaptic strength by mediating the rapid delivery, removal, and redistribution of synaptic AMPARs. Furthermore, by studying the real-time transport of C. elegans AMPAR subunits in vivo, we demonstrate that although homomeric GLR-1 AMPARs can diffuse to and accumulate at synapses in unc-116 mutants, glutamate-gated currents are diminished because heteromeric GLR-1/GLR-2 receptors do not reach synapses in the absence of UNC-116/KIF5-mediated transport. Our data support a model in which ongoing motor-driven delivery and removal of AMPARs controls not only the number but also the composition of synaptic AMPARs, and thus the strength of synaptic transmission.

Indexed as

AnimalsCaenorhabditis elegans ProteinsCell Cycle ProteinsCycloheximideGlutamic AcidKinesinsMembrane PotentialsMutationReceptors, AMPASynaptic TransmissionCaenorhabditis elegans ProteinsCell Cycle ProteinsCycloheximideglr-1 protein, C elegansGLR-2 protein, C elegansGlutamic AcidKinesinsKLP-4 protein, C elegansReceptors, AMPAUNC-116 protein, C elegans

Identifiers

PMID24360545
PMCPMC3933021

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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.