Evidence map›Paper›PMID 19772899›Full record

ArticleNeuroscience2009

5-HT2 receptors modulate excitatory neurotransmission to cardiac vagal neurons within the nucleus ambiguus evoked during and after hypoxia.

O Dergacheva, H Kamendi, X Wang, R A Pinol, J Frank, C Gorini, H Jameson, M R Lovett-Barr, D Mendelowitz

Abstract read
In one paragraph

Article in Neuroscience, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
0.8field-weighted citation impact, top 35% 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

7 citing papers in PubMed, 15 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

9 authors at 1 institution in 1 country.

O DergachevaDepartment of Pharmacology and Physiology, The George Washington University, 2300 Eye Street NW, Washington, DC 20037, USA. olgad@gwu.edu
H Kamendi
X Wang
R A Pinol
J Frank
C Gorini
H Jameson
M R Lovett-Barr
D Mendelowitz
George Washington University · US

Funding

Nicotine Modulation of Parasympathetic Cardiac NeuronsR01HL072006 · NHLBI · GEORGE WASHINGTON UNIVERSITY · PI MENDELOWITZ, DAVID · 2003 to 2017
$5.4M
NEUROPHYSIOLOGY OF PARASYMPATHETIC CARDIAC NEURONSR01HL049965 · NHLBI · UNIVERSITY OF TENNESSEE HEALTH SCI CTR · PI MENDELOWITZ, DAVID · 1998 to 2014
$4.6M
MECHANISM OF CARDIORESPIRATORY RHYTHM IN NEONATESR01HL059895 · NHLBI · UNIVERSITY OF TENNESSEE HEALTH SCI CTR · PI MENDELOWITZ, DAVID · 1998 to 2013
$4.1M
NHLBI NIH HHS R01 HL049965NHLBI NIH HHS R01 HL059895NHLBI NIH HHS R01 HL072006
6 · The paper itself

Abstract

To examine the role of 5-HT2 receptors in the central cardiorespiratory network, and in particular the respiratory modulation of parasympathetic activity to the heart, we used an in vitro medullary slice that allowed simultaneous examination of rhythmic inspiratory-related activity recorded from hypoglossal rootlet and excitatory inspiratory-related neurotransmission to cardioinhibitory vagal neurons (CVNs) within the nucleus ambiguus (NA). Focal application of ketanserin, a 5-HT2 receptor antagonist, did not significantly alter the frequency of spontaneous excitatory postsynaptic excitatory currents (EPSCs) in CVNs in control conditions. However, ketanserin diminished spontaneous excitatory neurotransmission to CVNs during hypoxia. The inhibitory action of ketanserin was on 5-HT3 mediated EPSCs during hypoxia since these responses were blocked by the 5-HT3 receptor antagonist ondansetron. In addition, a robust inspiratory-related excitatory neurotransmission was recruited during recovery from hypoxia. Focal application of ketanserin during this posthypoxia period evoked a significant augmentation of the frequency of inspiratory-related, but not spontaneous EPSCs in CVNs. This excitatory effect of ketanserin was prevented by application of the purinergic receptor blocker pyridoxal-phosphate-6-azophenyl-2',4'-disulfonic acid (PPADS). These results demonstrate 5-HT2 receptors differentially modulate excitatory neurotransmission to CVNs during and after hypoxia. Activation of 5-HT2 receptors acts to maintain excitatory neurotransmission to CVNs during hypoxia, likely via presynaptic facilitation of 5-HT3 receptor-mediated neurotransmission to CVNs. However, activation of 5HT2 receptors diminishes the subsequent inspiratory-related excitatory neurotransmission to CVNs that is recruited during the recovery from hypoxia likely exerting an inhibitory action on inspiratory-related purinergic signaling.

Indexed as

Purinergic AntagonistsAnimalsDisease Models, AnimalExcitatory Postsynaptic PotentialsHeartHypoxia, BrainKetanserinMedulla OblongataNeural InhibitionNeuronsOndansetronOrgan Culture TechniquesPyridoxal PhosphateRatsRats, Sprague-DawleyReceptors, PurinergicKetanserinOndansetronPurinergic AntagonistsPyridoxal Phosphatepyridoxal phosphate-6-azophenyl-2',4'-disulfonic acidReceptors, PurinergicReceptors, Serotonin, 5-HT2SerotoninSerotonin Antagonists

Identifiers

PMID19772899
PMCPMC2783201
OpenAlexW2071190305

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.