Evidence map›Paper›PMID 21734104›Full record

ArticleJournal of neurophysiology2011

Hydrogen sulfide augments synaptic neurotransmission in the nucleus of the solitary tract.

James R Austgen, Gerlinda E Hermann, Heather A Dantzler, Richard C Rogers, David D Kline

Open access · greenAbstract read
In one paragraph

Article in Journal of neurophysiology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed
2.4field-weighted citation impact, top 12% 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

35 citing papers in PubMed, 62 citations in OpenAlex.

  1. Review
  2. Hydrogen sulfide/polysulfides signaling and neuronal diseases.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2025
    Review
  3. Role of cystathionine-β-synthase and hydrogen sulfide in down syndrome.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2025
    Review
  4. Article
  5. Hydrogen Sulfide (HInternational journal of molecular sciences · 2025
    Review
  6. Review
  7. Article
  8. HFrontiers in chemistry · 2023
    Review
  9. Article
  10. Article
  11. Article
  12. Article
  13. Review
  14. Article
  15. Article
  16. A fluorescentChemical science · 2018
    Article
  17. Article
  18. Role of thiosulfate in hydrogen sulfide-dependent redox signaling in endothelial cells.American journal of physiology. Heart and circulatory physiology · 2017
    Article
  19. Article
  20. Article
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 2 institutions in 1 country.

James R AustgenDepartment of Biomedical Science, University of Missouri, Columbia, MO 65211, USA.
Gerlinda E Hermann
Heather A Dantzler
Richard C Rogers
David D Kline
University of Missouri · USPennington Biomedical Research Center · US

Funding

Adaptation of Brainstem Circuits to Chronic HypoxiaR01HL085108 · NHLBI · UNIVERSITY OF MISSOURI-COLUMBIA · PI KLINE, DAVID DOUGLAS · 2008 to 2012
$1.9M
NHLBI NIH HHS HL-085108
6 · The paper itself

Abstract

Within the brain stem, the nucleus tractus solitarii (NTS) serves as a principal central site for sensory afferent integration from the cardiovascular and respiratory reflexes. Neuronal activity and synaptic transmission in the NTS are highly pliable and subject to neuromodulation. In the central nervous system, hydrogen sulfide (H₂S) is a gasotransmitter generated primarily by the enzyme cystathionine-β-synthase (CBS). We sought to determine the role of H₂S, and its generation by CBS, in NTS excitability. Real-time RT-PCR, immunoblot, and immunohistochemistry analysis identified the presence of CBS in the NTS. Patch-clamp electrophysiology in brain stem slices examined excitatory postsynaptic currents (EPSCs) and membrane properties in monosynaptically driven NTS neurons. Confocal imaging of labeled afferent synaptic terminals in NTS slices monitored intracellular calcium. Exogenous H₂S significantly increased the amplitude of evoked solitary tract (TS)-EPSCs, frequency of miniature (m)EPSCs, and presynaptic terminal calcium fluorescence in the NTS. H₂S did not alter action potential discharge or postsynaptic properties. On the other hand, the CBS inhibitor aminooxyacetate (AOA) significantly reduced the amplitude of TS-EPSCs and presynaptic terminal calcium fluorescence in the NTS without altering postsynaptic properties. Taken together, these data support a presynaptic role for endogenous H₂S in modulation of excitatory neurotransmission in the NTS.

Indexed as

Aminooxyacetic AcidAnimalsCalcium SignalingCystathionine beta-SynthaseExcitatory Postsynaptic PotentialsHydrogen SulfideMaleNerve Tissue ProteinsPatch-Clamp TechniquesRatsRats, Sprague-DawleyReal-Time Polymerase Chain ReactionRNA, MessengerSolitary NucleusSynaptic TransmissionAminooxyacetic AcidCystathionine beta-SynthaseHydrogen SulfideNerve Tissue ProteinsRNA, Messenger

Identifiers

PMID21734104
PMCPMC3191839
OpenAlexW2153332286

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.