Evidence map›Paper›PMID 27330059›Full record

ArticleJournal of molecular cell biology2017

BDNF rescues prefrontal dysfunction elicited by pyramidal neuron-specific DTNBP1 deletion in vivo.

Wen Zhang, Kathryn M Daly, Bo Liang, Lifeng Zhang, Xuan Li, Yun Li, Da-Ting Lin

Open access · bronzeAbstract read
In one paragraph

Article in Journal of molecular cell biology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
0.5field-weighted citation impact, top 35% 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

15 citing papers in PubMed, 18 citations in OpenAlex.

  1. Single-dose psilocybin promotes cell-type-specific changes of neurons in the orbitofrontal cortex.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2026
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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

7 authors at 3 institutions in 1 country.

Wen ZhangIntramural Research Program, National Institute on Drug Abuse, National Institutes of Health, 333 Cassell Drive, Baltimore, MD 21224, USA.
Kathryn M DalyIntramural Research Program, National Institute on Drug Abuse, National Institutes of Health, 333 Cassell Drive, Baltimore, MD 21224, USA.
Bo LiangIntramural Research Program, National Institute on Drug Abuse, National Institutes of Health, 333 Cassell Drive, Baltimore, MD 21224, USA.
Lifeng ZhangIntramural Research Program, National Institute on Drug Abuse, National Institutes of Health, 333 Cassell Drive, Baltimore, MD 21224, USA.
Xuan LiIntramural Research Program, National Institute on Drug Abuse, National Institutes of Health, 333 Cassell Drive, Baltimore, MD 21224, USA.
Yun LiIntramural Research Program, National Institute on Drug Abuse, National Institutes of Health, 333 Cassell Drive, Baltimore, MD 21224, USA.
Da-Ting LinIntramural Research Program, National Institute on Drug Abuse, National Institutes of Health, 333 Cassell Drive, Baltimore, MD 21224, USA.
National Institutes of Health · USNational Institute on Drug Abuse · USJackson Laboratory · US

Funding

In vivo imaging of dorsal striatum function in freely behaving miceZIADA000603 · NIDA · NATIONAL INSTITUTE ON DRUG ABUSE · PI LIN, DA-TING · 2015 to 2025
$22.3M
6 · The paper itself

Abstract

Dystrobrevin-binding protein 1 (Dtnbp1) is one of the earliest identified schizophrenia susceptibility genes. Reduced expression of DTNBP1 is commonly found in brain areas of schizophrenic patients. Dtnbp1-null mutant mice exhibit abnormalities in behaviors and impairments in neuronal activities. However, how diminished DTNBP1 expression contributes to clinical relevant features of schizophrenia remains to be illustrated. Here, using a conditional Dtnbp1 knockout mouse line, we identified an in vivo schizophrenia-relevant function of DTNBP1 in pyramidal neurons of the medial prefrontal cortex (mPFC). We demonstrated that DTNBP1 elimination specifically in pyramidal neurons of the mPFC impaired mouse pre-pulse inhibition (PPI) behavior and reduced perisomatic GABAergic synapses. We further revealed that loss of DTNBP1 in pyramidal neurons diminished activity-dependent secretion of brain-derived neurotrophic factor (BDNF). Finally, we showed that chronic BDNF infusion in the mPFC fully rescued both GABAergic synaptic dysfunction and PPI behavioral deficit induced by DTNBP1 elimination from pyramidal neurons. Our findings highlight brain region- and cell type-specific functions of DTNBP1 in the pathogenesis of schizophrenia, and underscore BDNF restoration as a potential therapeutic strategy for schizophrenia.

Indexed as

Gene DeletionAnimalsBehavior, AnimalBrain-Derived Neurotrophic FactorDependovirusDysbindinDystrophin-Associated ProteinsExcitatory Postsynaptic Potentialsgamma-Aminobutyric AcidGreen Fluorescent ProteinsInhibitory Postsynaptic PotentialsIntegrasesMaleMiceOrgan SpecificityPrefrontal CortexBrain-Derived Neurotrophic FactorCre recombinaseDtnbp1 protein, mouseDysbindinDystrophin-Associated Proteinsenhanced green fluorescent proteingamma-Aminobutyric AcidGreen Fluorescent ProteinsIntegrasesBDNFdisinhibitionDtnbp1GABAergicPFCschizophrenia

Identifiers

PMID27330059
PMCPMC6080364
OpenAlexW2460190855

What OpenQuestion holds

Textmetadata
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.