Evidence map›Paper›PMID 33589740›Full record

ArticleMolecular psychiatry2021

Dysbindin-1 regulates mitochondrial fission and gamma oscillations.

Jun Zhao, Huiwen Zhu, Kaizheng Duan, Ronald S Petralia, Ya-Xian Wang, Qinhua Gu, Debabrata Panja, Zheng Li

Open access · hybridAbstract read
In one paragraph

Article in Molecular psychiatry, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
0.6field-weighted citation impact, top 34% 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

9 citing papers in PubMed, 12 citations in OpenAlex.

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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

8 authors at 1 institution in 1 country.

Jun Zhao *Section on Synapse Development Plasticity, National Institute of Mental Health, National Institutes of Health, Bethesda, Maryland, United States.
Huiwen Zhu *Section on Synapse Development Plasticity, National Institute of Mental Health, National Institutes of Health, Bethesda, Maryland, United States.
Kaizheng DuanSection on Synapse Development Plasticity, National Institute of Mental Health, National Institutes of Health, Bethesda, Maryland, United States.
Ronald S PetraliaAdvanced Imaging Core, National Institute on Deafness and Other Communication Disorders, National Institutes of Health, Bethesda, Maryland, United States.
Ya-Xian WangAdvanced Imaging Core, National Institute on Deafness and Other Communication Disorders, National Institutes of Health, Bethesda, Maryland, United States.
Qinhua GuSection on Synapse Development Plasticity, National Institute of Mental Health, National Institutes of Health, Bethesda, Maryland, United States.
Debabrata PanjaSection on Synapse Development Plasticity, National Institute of Mental Health, National Institutes of Health, Bethesda, Maryland, United States.ORCID http://orcid.org/0000-0003-4774-1167
Zheng LiSection on Synapse Development Plasticity, National Institute of Mental Health, National Institutes of Health, Bethesda, Maryland, United States. lizheng2@mail.nih.gov.ORCID http://orcid.org/0000-0002-2978-2531
National Institutes of Health · US

Funding

Non-apoptotic function of casapses in synapsesZIAMH002881 · NIMH · NATIONAL INSTITUTE OF MENTAL HEALTH · PI LI, ZHENG · 2009 to 2025
$18.9M
Advanced Imaging CoreZICDC000081 · NIDCD · NATIONAL INSTITUTE ON DEAFNESS AND OTHER COMMUNICATION DISORDERS · PI WINKLER, DENNIS · 2012 to 2025
$17.4M
Intramural NIH HHS ZIA MH002881Intramural NIH HHS ZIC DC000081
6 · The paper itself

Abstract

Mitochondria are cellular ATP generators. They are dynamic structures undergoing fission and fusion. While much is known about the mitochondrial fission machinery, the mechanism of initiating fission and the significance of fission to neurophysiology are largely unclear. Gamma oscillations are synchronized neural activities that impose a great energy challenge to synapses. The cellular mechanism of fueling gamma oscillations has yet to be defined. Here, we show that dysbindin-1, a protein decreased in the brain of individuals with schizophrenia, is required for neural activity-induced fission by promoting Drp1 oligomerization. This process is engaged by gamma-frequency activities and in turn, supports gamma oscillations. Gamma oscillations and novel object recognition are impaired in dysbindin-1 null mice. These defects can be ameliorated by increasing mitochondrial fission. These findings identify a molecular mechanism for activity-induced mitochondrial fission, a role of mitochondrial fission in gamma oscillations, and mitochondrial fission as a potential target for improving cognitive functions.

Indexed as

MitochondriaMitochondrial DynamicsAnimalsDynaminsDysbindinMiceMice, KnockoutMitochondrial ProteinsSynapsesDynaminsDysbindinMitochondrial Proteins

Identifiers

PMID33589740
PMCPMC8364574
OpenAlexW3130631209

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.