Evidence map›Paper›PMID 29088700›Full record

ArticleNature2017

Synaptotagmin 7 confers frequency invariance onto specialized depressing synapses.

Josef Turecek, Skyler L Jackman, Wade G Regehr

Open access · greenAbstract read
In one paragraph

Article in Nature, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 papers.

0numbers the graph read from it
0cells of the map it votes in
57citing papers in PubMed
4.2field-weighted citation impact, top 5% of its field
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

57 citing papers in PubMed, 105 citations in OpenAlex.

  1. Alternative splicing of synaptotagmin 7 regulates oligomerization and short-term synaptic plasticity.Proceedings of the National Academy of Sciences of the United States of America · 2026
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  8. A metal-organic framework neuron.National science review · 2025
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  10. The cerebellar deep nuclei: a patch for rate codes?Frontiers in neural circuits · 2025
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  14. Synaptotagmin 7 Sculpts Short-Term Plasticity at a High Probability Synapse.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2024
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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

3 authors at 1 institution in 1 country.

Josef Turecek1Department of Neurobiology, Harvard Medical School, 220 Longwood Avenue, Boston, Massachusetts 02115, USA.
Skyler L Jackman1Department of Neurobiology, Harvard Medical School, 220 Longwood Avenue, Boston, Massachusetts 02115, USA.
Wade G Regehr1Department of Neurobiology, Harvard Medical School, 220 Longwood Avenue, Boston, Massachusetts 02115, USA.
Harvard University · US

Funding

Viral ModuleP30EY012196 · NEI · HARVARD UNIVERSITY (MEDICAL SCHOOL) · PI ZHIGANG HE · 1998 to 2026
$21.3M
Mechanisms and Functions of Synapses and CircuitsR35NS097284 · NINDS · HARVARD MEDICAL SCHOOL · PI REGEHR, WADE G · 2017 to 2024
$7.5M
Super-Resolution ImagingP30NS072030 · NINDS · HARVARD MEDICAL SCHOOL · PI REGEHR, WADE G · 2011 to 2020
$5.8M
Short-Term Synaptic Plasticity in the CNSR01NS032405 · NINDS · HARVARD UNIVERSITY (MEDICAL SCHOOL) · PI REGEHR, WADE G · 1995 to 2016
$4.8M
NEI NIH HHS P30 EY012196NINDS NIH HHS P30 NS072030NINDS NIH HHS R01 NS032405NINDS NIH HHS R35 NS097284
6 · The paper itself

Abstract

At most synapses in the brain, short-term plasticity dynamically modulates synaptic strength. Rapid frequency-dependent changes in synaptic strength have key roles in sensory adaptation, gain control and many other neural computations. However, some auditory, vestibular and cerebellar synapses maintain constant strength over a wide range of firing frequencies, and as a result efficiently encode firing rates. Despite its apparent simplicity, frequency-invariant transmission is difficult to achieve because of inherent synaptic nonlinearities. Here we study frequency-invariant transmission at synapses from Purkinje cells to deep cerebellar nuclei and at vestibular synapses in mice. Prolonged activation of these synapses leads to initial depression, which is followed by steady-state responses that are frequency invariant for their physiological activity range. We find that synaptotagmin 7 (Syt7), a calcium sensor for short-term facilitation, is present at both synapses. It was unclear why a sensor for facilitation would be present at these and other depressing synapses. We find that at Purkinje cell and vestibular synapses, Syt7 supports facilitation that is normally masked by depression, which can be revealed in wild-type mice but is absent in Syt7 knockout mice. In wild-type mice, facilitation increases with firing frequency and counteracts depression to produce frequency-invariant transmission. In Syt7-knockout mice, Purkinje cell and vestibular synapses exhibit conventional use-dependent depression, weakening to a greater extent as the firing frequency is increased. Presynaptic rescue of Syt7 expression restores both facilitation and frequency-invariant transmission. Our results identify a function for Syt7 at synapses that exhibit overall depression, and demonstrate that facilitation has an unexpected and important function in producing frequency-invariant transmission.

Indexed as

Neural InhibitionNeuronal PlasticitySynaptic TransmissionAnimalsAuditory PerceptionCalciumCerebellumFemaleMaleMiceMice, KnockoutPresynaptic TerminalsPurkinje CellsSynapsesSynaptotagminsVestibule, LabyrinthCalciumSynaptotagmins

Identifiers

PMID29088700
PMCPMC5892411
OpenAlexW2765649616

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

None linked

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.