Evidence map›Paper›PMID 26241953›Full record

ArticlePloS one2015

Activity-Dependent Bidirectional Regulation of GAD Expression in a Homeostatic Fashion Is Mediated by BDNF-Dependent and Independent Pathways.

Yoko Hanno-Iijima, Masami Tanaka, Takatoshi Iijima

Open access · goldAbstract readComparative Study
In one paragraph

Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.5field-weighted citation impact, top 19% 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

16 citing papers in PubMed, 27 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

3 authors at 1 institution in 1 country.

Yoko Hanno-IijimaTokai University Institute of Innovative Science and Technology, Medical Division, Kanagawa, Japan; School of Medicine, Tokai University, Kanagawa, Japan.
Masami TanakaTokai University Institute of Innovative Science and Technology, Medical Division, Kanagawa, Japan; School of Medicine, Tokai University, Kanagawa, Japan.
Takatoshi IijimaTokai University Institute of Innovative Science and Technology, Medical Division, Kanagawa, Japan; School of Medicine, Tokai University, Kanagawa, Japan.
Tokai University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Homeostatic synaptic plasticity, or synaptic scaling, is a mechanism that tunes neuronal transmission to compensate for prolonged, excessive changes in neuronal activity. Both excitatory and inhibitory neurons undergo homeostatic changes based on synaptic transmission strength, which could effectively contribute to a fine-tuning of circuit activity. However, gene regulation that underlies homeostatic synaptic plasticity in GABAergic (GABA, gamma aminobutyric) neurons is still poorly understood. The present study demonstrated activity-dependent dynamic scaling in which NMDA-R (N-methyl-D-aspartic acid receptor) activity regulated the expression of GABA synthetic enzymes: glutamic acid decarboxylase 65 and 67 (GAD65 and GAD67). Results revealed that activity-regulated BDNF (brain-derived neurotrophic factor) release is necessary, but not sufficient, for activity-dependent up-scaling of these GAD isoforms. Bidirectional forms of activity-dependent GAD expression require both BDNF-dependent and BDNF-independent pathways, both triggered by NMDA-R activity. Additional results indicated that these two GAD genes differ in their responsiveness to chronic changes in neuronal activity, which could be partially caused by differential dependence on BDNF. In parallel to activity-dependent bidirectional scaling in GAD expression, the present study further observed that a chronic change in neuronal activity leads to an alteration in neurotransmitter release from GABAergic neurons in a homeostatic, bidirectional fashion. Therefore, the differential expression of GAD65 and 67 during prolonged changes in neuronal activity may be implicated in some aspects of bidirectional homeostatic plasticity within mature GABAergic presynapses.

Indexed as

Gene Expression RegulationAnimalsBenzenesulfonamidesBenzylaminesBicucullineBrain-Derived Neurotrophic FactorButadienesCalcium SignalingCarbazolesCells, CulturedCerebral CortexEnzyme InductionGABAergic Neuronsgamma-Aminobutyric AcidGlutamate DecarboxylaseHomeostasisBenzenesulfonamidesBenzylaminesBicucullineBrain-Derived Neurotrophic FactorButadienesCarbazolesgamma-Aminobutyric AcidGlutamate Decarboxylaseglutamate decarboxylase 1glutamate decarboxylase 2Indole AlkaloidsKN 93NitrilesProtein IsoformsProtein Kinase InhibitorsReceptors, N-Methyl-D-AspartateReceptor, trkBRNA, Messengerstaurosporine aglyconeSulfonamidesU 0126

Identifiers

PMID26241953
PMCPMC4524701
OpenAlexW2199612419

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.