Evidence map›Paper›PMID 21771639›Full record

ArticleNeuroscience2011

α1-adrenergic receptors facilitate inhibitory neurotransmission to cardiac vagal neurons in the nucleus ambiguus.

C R Boychuk, R J Bateman, K E Philbin, D Mendelowitz

Abstract read
In one paragraph

Article in Neuroscience, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed, 1 pooled it
1.4field-weighted citation impact, top 21% 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

17 citing papers in PubMed, 1 synthesis or guideline pooled it, 24 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Chemogenetic activation of noradrenergic A5 neurons increases blood pressure and visceral sympathetic activity in adult rats.American journal of physiology. Regulatory, integrative and comparative physiology · 2022
    Article
  4. Review
  5. Article
  6. Article
  7. Parasympathetic Vagal Control of Cardiac Function.Current hypertension reports · 2016
    Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Cardiorespiratory coupling in health and disease.Autonomic neuroscience : basic & clinical · 2013
    Review
  15. Article
  16. Article
  17. 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

4 authors at 1 institution in 1 country.

C R BoychukDepartment of Pharmacology and Physiology, The George Washington University, 2300 Eye Street Northwest, Washington, DC 20037, USA.
R J Bateman
K E Philbin
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
NEUROPHYSIOLOGY OF PARASYMPATHETIC CARDIAC NEURONSR29HL049965 · NHLBI · UNIVERSITY OF TENNESSEE HEALTH SCI CTR · PI MENDELOWITZ, DAVID · 1993 to 1997
–
NHLBI NIH HHS HL49965NHLBI NIH HHS R01 HL049965NHLBI NIH HHS R01 HL059895NHLBI NIH HHS R01 HL072006PHS HHS 59895PHS HHS 72006PHS HHS SLORR025565
6 · The paper itself

Abstract

The cholinergic cardiac vagal neurons (CVNs), located in the nucleus ambiguus, are the origin of cardioinhibitory parasympathetic activity. Catecholaminergic neurons in nearby regions of the brainstem, including the C1 and C2 cell groups, are thought to play a key role in both arousing from sleep and maintaining wakefulness. Because norepinephrine (NE) could play an important role in influencing the activity of CVNs, particularly in response to sleeping/waking and arousal states, the present study investigated the contribution of α(1)-adrenergic receptor activation to augment inhibitory and/or blunt excitatory neurotransmission to CVNs. To test the effects of α(1)-adrenergic receptor activation, CVNs were labeled in rats by retrograde tracing and synaptic events were recorded by whole cell voltage clamp techniques in vitro. Prazosin, an inverse agonist of α(1)-adrenergic receptor, significantly decreased the frequency of both GABAergic and glycinergic neurotransmission to CVNs. Activation of α(1)-adrenergic receptors by the α(1)-adrenergic receptor agonists NE or phenylephrine (PE) both significantly increased GABAergic and glycinergic inhibitory event frequency. This effect was prevented by the sodium channel blocker tetrodotoxin (TTX). Activation of α(1)-adrenergic receptors did not alter glutamatergic neurotransmission to CVNs. This study indicates that α(1)-adrenergic receptor activation in the brainstem can facilitate inhibitory GABAergic and glycinergic neurotransmission so as to reduce CVN activity; this synaptic modulation may play a role in the tachycardia seen during NE-dependent behavioral arousal.

Indexed as

Adrenergic AgentsAnimalsAnimals, Newborngamma-Aminobutyric AcidGlycineInhibitory Postsynaptic PotentialsNeural InhibitionNeuronsNorepinephrineNucleus AccumbensRatsRats, Sprague-DawleyReceptors, Adrenergic, alpha-1Sodium Channel BlockersTetrodotoxinTyrosine 3-MonooxygenaseAdrenergic Agentsgamma-Aminobutyric AcidGlycineNorepinephrineReceptors, Adrenergic, alpha-1Sodium Channel BlockersTetrodotoxinTyrosine 3-Monooxygenase

Identifiers

PMID21771639
PMCPMC3171606
OpenAlexW1964885699

What OpenQuestion holds

Textmetadata
LicenceTDM
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.