Evidence map›Paper›PMID 30601692›Full record

ArticleJournal of neurophysiology2019

TRPV1 channels contribute to spontaneous glutamate release in nucleus tractus solitarii following chronic intermittent hypoxia.

David D Kline, Sheng Wang, Diana L Kunze

Open access · bronzeAbstract read
In one paragraph

Article in Journal of neurophysiology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
0.8field-weighted citation impact, top 34% 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

19 citing papers in PubMed, 27 citations in OpenAlex.

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  10. Hypoxia augments TRPM3-mediated calcium influx in vagal sensory neurons.Autonomic neuroscience : basic & clinical · 2023
    Article
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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 2 institutions in 1 country.

David D KlineDepartment of Biomedical Sciences, University of Missouri , Columbia, Missouri.ORCID 0000-0003-3269-0184
Sheng WangDepartment of Neurosciences, Case Western Reserve University , Cleveland, Ohio.
Diana L KunzeDepartment of Neurosciences, Case Western Reserve University , Cleveland, Ohio.
MetroHealth · USUniversity of Missouri · US

Funding

Neurophysiology and plasticity of cardiorespiratory circuits to hypoxiaR01HL128454 · NHLBI · UNIVERSITY OF MISSOURI-COLUMBIA · PI KLINE, DAVID DOUGLAS · 2016 to 2019
$2.0M
Mechanism of Homeostatic Plasticity in a Visceral Sensory CircuitR01HL090886 · NHLBI · CASE WESTERN RESERVE UNIVERSITY · PI KUNZE, DIANA L · 2009 to 2010
$809k
NHLBI NIH HHS R01 HL090886NHLBI NIH HHS R01 HL128454
6 · The paper itself

Abstract

Chronic intermittent hypoxia (CIH) reduces afferent-evoked excitatory postsynaptic currents (EPSCs) but enhances basal spontaneous (s) and asynchronous (a) EPSCs in second-order neurons of nucleus tractus solitarii (nTS), a major area for cardiorespiratory control. The net result is an increase in synaptic transmission. The mechanisms by which this occurs are unknown. The N-type calcium channel and transient receptor potential cation channel TRPV1 play prominent roles in nTS sEPSCs and aEPSCs. The functional role of these channels in CIH-mediated afferent-evoked EPSC, sEPSC, and aEPSC was tested in rat nTS slices following antagonist inhibition and in mouse nTS slices that lack TRPV1. Block of N-type channels decreased aEPSCs in normoxic and, to a lesser extent, CIH-exposed rats. sEPSCs examined in the presence of TTX (miniature EPSCs) were also decreased by N-type block in normoxic but not CIH-exposed rats. Antagonist inhibition of TRPV1 reduced the normoxic and the CIH-mediated increase in sEPSCs, aEPSCs, and mEPSCs. As in rats, in TRPV1

Indexed as

AnimalsExcitatory Postsynaptic PotentialsGlutamic AcidHypoxiaMaleMiceMice, Inbred C57BLMiniature Postsynaptic PotentialsRatsRats, Sprague-DawleySolitary NucleusTRPV Cation ChannelsGlutamic AcidTRPV1 protein, mouseTRPV Cation Channelsautonomic nervous systemcalcium channelsintermittent hypoxiarespirationsynaptic transmission

Identifiers

PMID30601692
PMCPMC6520621
OpenAlexW2907151025

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.