Evidence map›Paper›PMID 21865474›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2011

Endogenous brain-derived neurotrophic factor in the nucleus tractus solitarius tonically regulates synaptic and autonomic function.

Catharine G Clark, Eileen M Hasser, Diana L Kunze, David M Katz, David D Kline

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
45citing papers in PubMed, 1 pooled it
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

45 citing papers in PubMed, 1 synthesis or guideline pooled it, 79 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.

Catharine G ClarkDalton Cardiovascular Research Center, Department of Biomedical Sciences, University of Missouri, Columbia, Missouri 65211, USA.
Eileen M Hasser
Diana L Kunze
David M Katz
David D Kline
Case Western Reserve University · USUniversity of Missouri · USCardiovascular Research Center · BR

Funding

Respiratory Circuit Dysfunction in Rett SyndromeR01NS057398 · NINDS · CASE WESTERN RESERVE UNIVERSITY · PI KATZ, DAVID M. · 2007 to 2013
$3.1M
Cardiovascular Regulation in Hindlimb Unweighted RatsR01HL055306 · NHLBI · UNIVERSITY OF MISSOURI-COLUMBIA · PI HASSER, EILEEN M · 1997 to 2010
$2.8M
Exercise &Health: Integration from Molecule to PatientT32AR048523 · NIAMS · UNIVERSITY OF MISSOURI-COLUMBIA · PI TERJUNG, RONALD L · 2003 to 2013
$2.5M
Adaptation of Brainstem Circuits to Chronic HypoxiaR01HL085108 · NHLBI · UNIVERSITY OF MISSOURI-COLUMBIA · PI KLINE, DAVID DOUGLAS · 2008 to 2012
$1.9M
Prefrontal cortical dysfunction in Rett syndromeR56NS057398 · NINDS · CASE WESTERN RESERVE UNIVERSITY · PI KATZ, DAVID M. · 2016 to 2016
$396k
NHLBI NIH HHS HL-085108NHLBI NIH HHS HL-55306NHLBI NIH HHS R01 HL055306NHLBI NIH HHS R01 HL085108NIAMS NIH HHS 5T32AR048523-05NIAMS NIH HHS T32 AR048523NINDS NIH HHS NS-057398NINDS NIH HHS R01 NS057398NINDS NIH HHS R56 NS057398
6 · The paper itself

Abstract

Brain-derived neurotrophic factor (BDNF) and its receptor, TrkB, are highly expressed in the nucleus tractus solitarius (nTS), the principal target of cardiovascular primary afferent input to the brainstem. However, little is known about the role of BDNF signaling in nTS in cardiovascular homeostasis. We examined whether BDNF in nTS modulates cardiovascular function in vivo and regulates synaptic and/or neuronal activity in isolated brainstem slices. Microinjection of BDNF into the rat medial nTS (mnTS), a region critical for baroreflex control of sympathetic outflow, produced dose-dependent increases in mean arterial pressure (MAP), heart rate (HR), and lumbar sympathetic nerve activity (LSNA) that were blocked by the tyrosine kinase inhibitor K252a. In contrast, immunoneutralization of endogenous BDNF (anti-BDNF), or microinjection of K252a alone, decreased MAP, HR, and LSNA. The effects of anti-BDNF were abolished by blockade of ionotropic glutamate receptors, indicating a role for glutamate signaling in the response to BDNF. In vitro, BDNF reduced the amplitude of miniature EPSCs as well as solitary tract (TS) evoked EPSC amplitude and action potential discharge (APD) in second-order nTS neurons. BDNF effects on EPSCs were independent of GABAergic signaling and abolished by AMPA receptor blockade. In contrast, K252a increased spontaneous EPSC frequency and TS evoked EPSC amplitude. BDNF also attenuated APD evoked by injection of depolarizing current into second-order neurons, indicating reduced intrinsic neuronal excitability. Our data demonstrate that BDNF signaling in mnTS plays a tonic role in regulating cardiovascular function, likely via modulation of primary afferent glutamatergic excitatory transmission and neural activity.

Indexed as

Cardiovascular Physiological PhenomenaAction PotentialsAnimalsAutonomic PathwaysBrain-Derived Neurotrophic FactorMaleNeuronsOrgan Culture TechniquesRatsRats, Sprague-DawleySolitary NucleusSynaptic TransmissionBrain-Derived Neurotrophic Factor

Identifiers

PMID21865474
PMCPMC3408222
OpenAlexW2096452233

What OpenQuestion holds

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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.