Evidence map›Paper›PMID 12122142›Full record

ArticleThe Journal of physiology2002

Neurotrophin modulation of voltage-gated potassium channels in rat through TrkB receptors is time and sensory experience dependent.

K Tucker, D A Fadool

Open access · greenAbstract read
In one paragraph

Article in The Journal of physiology, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 60 papers.

0numbers the graph read from it
0cells of the map it votes in
60citing papers in PubMed
1.6field-weighted citation impact, top 18% 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

60 citing papers in PubMed, 103 citations in OpenAlex.

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  13. Modulating the Excitability of Olfactory Output Neurons Affects Whole-Body Metabolism.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2022
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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.

K TuckerFlorida State University, Department of Biological Science, Program in Neuroscience and Molecular Biophysics, Biomedical Research Facility, Tallahassee, FL 32306, USA.
D A Fadool
Florida State University · US

Funding

MODULATION OF OLFACTORY BULB NEURON CURRENT PROPERTIESR29DC003387 · NIDCD · FLORIDA STATE UNIVERSITY · PI FADOOL, DEBRA ANN · 1998 to 2002
$333k
NIDCD NIH HHS R29 DC003387NIDCD NIH HHS R29 DC03387
6 · The paper itself

Abstract

The whole-cell configuration of the patch-clamp technique, immunoprecipitation experiments and unilateral naris occlusions were used to investigate whether the voltage-gated potassium channel Kv1.3 was a substrate for neurotrophin-induced tyrosine phosphorylation and subsequent functional modulation of current properties in cultured rat olfactory bulb (OB) neurons. Membrane proteins of the OB included all three Trk receptor kinases, but the truncated form of the receptor, lacking an intact kinase domain, was the predominant form of the protein for TrkA and TrkC, while TrkB was predominantly found as the full-length receptor. Acute (15 min) stimulation of OB neurons with bath application of 50 ng ml(-1) brain-derived neurotrophic factor (BDNF), which is a selective ligand for TrkB, caused suppression of the whole-cell outward current and no changes in the kinetics of inactivation or deactivation. Acute stimulation with either nerve growth factor or neurotrophin-3 failed to evoke any changes in Kv1.3 function in the OB neurons. Chronic exposure to BDNF (days) caused an increase in the magnitude of Kv1.3 current and speeding of the inactivation and deactivation of the channel. Acute BDNF-induced activation of TrkB receptors significantly increased tyrosine phosphorylation of Kv1.3 in the OB, as shown using a combined immunoprecipitation and Western blot analysis. With unilateral naris occlusion, the acute BDNF-induced tyrosine phosphorylation of Kv1.3 was increased in neurons lacking odour sensory experience. In summary, the duration of neurotrophin exposure and the sensory-dependent state of a neuron can influence the degree of phosphorylation of a voltage-gated ion channel and its concomitant functional modulation by neurotrophins.

Indexed as

Potassium Channels, Voltage-GatedAmino Acid SequenceAnimalsAnimals, NewbornBrain-Derived Neurotrophic FactorCell MembraneCells, CulturedElectric StimulationHumansImmune SeraIn Vitro TechniquesKv1.3 Potassium ChannelMembrane PotentialsMolecular Sequence DataNeuronsOlfaction DisordersBrain-Derived Neurotrophic FactorImmune SeraKCNA3 protein, humanKcna3 protein, ratKv1.3 Potassium ChannelPotassium ChannelsPotassium Channels, Voltage-GatedReceptors, Nerve Growth FactorReceptor, trkBRecombinant Proteins

Identifiers

PMID12122142
PMCPMC2290412
OpenAlexW2135478323

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.