Evidence map›Paper›PMID 34526080›Full record

ArticleMolecular brain2021

Brain-derived neurotrophic factor produced long-term synaptic enhancement in the anterior cingulate cortex of adult mice.

Hui-Hui Miao, Zhuang Miao, Ji-Gang Pan, Xu-Hui Li, Min Zhuo

Open access · goldAbstract read
In one paragraph

Article in Molecular brain, 2021. 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
2.2field-weighted citation impact, top 13% 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, 29 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

5 authors at 3 institutions in 2 countries.

Hui-Hui MiaoDepartment of Anesthesiology, Beijing Shijitan Hospital, Capital Medical University, Beijing, 100038, People's Republic of China.
Zhuang MiaoDepartment of Physiology, Faculty of Medicine, University of Toronto, Medical Science Building, 1 King's College Circle, Toronto, ON, M5S 1A8, Canada.
Ji-Gang PanDepartment of Physiology, Faculty of Medicine, University of Toronto, Medical Science Building, 1 King's College Circle, Toronto, ON, M5S 1A8, Canada.
Xu-Hui LiDepartment of Physiology, Faculty of Medicine, University of Toronto, Medical Science Building, 1 King's College Circle, Toronto, ON, M5S 1A8, Canada. lixuhui0207@163.com.ORCID 0000-0003-4376-6252
Min ZhuoDepartment of Physiology, Faculty of Medicine, University of Toronto, Medical Science Building, 1 King's College Circle, Toronto, ON, M5S 1A8, Canada. min.zhuo@utoronto.ca.
University of Toronto · CACapital Medical University · CNQingdao University · CN

Funding

CIHR PJT-148648CIHR PJT-419286
6 · The paper itself

Abstract

Previous studies have demonstrated that brain-derived neurotrophic factor (BDNF) is one of the diffusible messengers for enhancing synaptic transmission in the hippocampus. Less information is available about the possible roles of BDNF in the anterior cingulate cortex (ACC). In the present study, we used 64-electrode array field recording system to investigate the effect of BDNF on ACC excitatory transmission. We found that BDNF enhanced synaptic responses in a dose-dependent manner in the ACC in C57/BL6 mice. The enhancement was long-lasting, and persisted for at least 3 h. In addition to the enhancement, BDNF also recruited inactive synaptic responses in the ACC. Bath application of the tropomyosin receptor kinase B (TrkB) receptor antagonist K252a blocked BDNF-induced enhancement. L-type voltage-gated calcium channels (L-VGCC), metabotropic glutamate receptors (mGluRs), but not NMDA receptors were required for BDNF-produced enhancement. Moreover, calcium-stimulated adenylyl cyclase subtype 1 (AC1) but not AC8 was essential for the enhancement. A selective AC1 inhibitor NB001 completely blocked the enhancement. Furthermore, BDNF-produced enhancement occluded theta burst stimulation (TBS) induced long-term potentiation (LTP), suggesting that they may share similar signaling mechanisms. Finally, the expression of BDNF-induced enhancement depends on postsynaptic incorporation of calcium-permeable AMPA receptors (CP-AMPARs) and protein kinase Mζ (PKMζ). Our results demonstrate that cortical BDNF may contribute to synaptic potentiation in the ACC.

Indexed as

Adenosine TriphosphateAdenylyl CyclasesAnimalsBrain-Derived Neurotrophic FactorCalcium Channels, L-TypeCarbazolesDose-Response Relationship, DrugElectrodes, ImplantedGyrus CinguliIndole AlkaloidsLong-Term PotentiationMaleMiceMice, Inbred C57BLProtein Kinase CProtein Kinase C zeta5-((2-(6-Amino-9H-purin-9-yl) ethyl) amino)-1-pentanolAdenosine Triphosphateadenylyl cyclase 1Adenylyl CyclasesBrain-Derived Neurotrophic FactorCalcium Channels, L-TypeCarbazolesIndole AlkaloidsProtein Kinase CProtein Kinase C zetaReceptors, AMPAReceptors, Metabotropic Glutamatestaurosporine aglyconeAdenylyl cyclase subtype 1AMPAAnterior cingulate cortexBrain-derived neurotrophic factorLTP

Identifiers

PMID34526080
PMCPMC8442386
OpenAlexW3196007322

What OpenQuestion holds

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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.