Evidence map›Paper›PMID 12640011›Full record

ArticleThe Journal of physiology2003

Brain-derived neurotrophic factor attenuates mouse cerebellar granule cell GABA(A) receptor-mediated responses via postsynaptic mechanisms.

Qing Cheng, Hermes H Yeh

Open access · greenAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in The Journal of physiology, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
2.5field-weighted citation impact, top 11% 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

32 citing papers in PubMed, 75 citations in OpenAlex.

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  9. Mechanism of GABA receptors involved in spasticity inhibition induced by transcranial magnetic stimulation following spinal cord injury.Journal of Huazhong University of Science and Technology. Medical sciences = Hua zhong ke ji da xue xue bao. Yi xue Ying De wen ban = Huazhong keji daxue xuebao. Yixue Yingdewen ban · 2015
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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

2 authors at 1 institution in 1 country.

Qing ChengCenter for Aging and Developmental Biology, Department of Pharmacology and Physiology, University of Rochester Medical Center, 601 Elmwood Avenue, Rochester, NY 14642, USA.
Hermes H Yeh
University of Rochester Medical Center · US

Funding

Development of the Cerebral Cortex in MammalsR01NS041489 · NINDS · UNIVERSITY OF CONNECTICUT SCH OF MED/DNT · PI ZECEVIC, NADA R · 2001 to 2013
$3.8M
STUDIES OF CNS PEPTIDES IN CELL CULTURER01NS024830 · NINDS · WAKE FOREST UNIVERSITY · PI YEH, HERMES H. · 1987 to 1999
–
NINDS NIH HHS NS24830NINDS NIH HHS NS41489NINDS NIH HHS R01 NS041489
6 · The paper itself

Abstract

In addition to exerting long-term neurotrophic influences on developmental process such as neuronal survival and neuritic outgrowth, brain-derived neurotrophic factor (BDNF) has been reported to modulate synaptic transmission in the short-term. Considerable evidence indicates that BDNF acutely modulates NMDA receptor-mediated synaptic activity. However, whether BDNF modulates inhibitory synaptic transmission remains to be firmly established. In the present study, we examined the effect of acute BDNF exposure on GABA-evoked whole-cell responses as well as GABAergic synaptic activity in cultured mouse cerebellar granule cells. GABA-evoked responses were reduced by 39.5 +/- 4.7 % upon acute and focal application of BDNF (100 ng ml-1). The reduction of the GABA response recovered only partially even minutes after removal of BDNF. TrkB-IgG and K252a, but not K252b, prevented the BDNF-induced attenuation of the GABA response. BDNF exposure shifted the cumulative peak amplitude distribution leftward for both spontaneous IPSCs (sIPSCs) and miniature IPSCs (mIPSCs) without affecting the rise time and decay time constants. Acute exposure to BDNF also resulted in internalization of GABAA receptors in cultured cerebellar granule cells, as reflected by diminished immunostaining with an antibody against the GABAA receptor beta2/3 subunit. Although the BDNF-induced GABAA receptor internalization was sensitive to K252a, it did not become manifest until 5 min after exposure to BDNF. Therefore, receptor internalization alone cannot account for the prompt BDNF-induced attenuation of GABA-mediated activity. We conclude that BDNF modulates GABAA receptor-mediated activity through TrkB receptor signalling that triggers a kinase-dependent short latency effect and a delayed longer latency effect hallmarked by receptor internalization.

Indexed as

AnimalsBrain-Derived Neurotrophic FactorCells, CulturedCerebellumEvoked Potentialsgamma-Aminobutyric AcidMiceNeuronsPatch-Clamp TechniquesReceptors, GABA-AReceptor, trkBSignal TransductionSynapsesBrain-Derived Neurotrophic Factorgamma-Aminobutyric AcidReceptors, GABA-AReceptor, trkB

Identifiers

PMID12640011
PMCPMC2342883
OpenAlexW1979306444

What Socratic 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 Socratic graph.