Evidence map›Paper›PMID 21613611›Full record

ArticleAmerican journal of physiology. Cell physiology2011

Mechanisms of facilitation of synaptic glutamate release by nicotinic agonists in the nucleus of the solitary tract.

Bopanna I Kalappa, Lin Feng, William R Kem, Alexander G Gusev, Victor V Uteshev

Open access · greenAbstract read
In one paragraph

Article in American journal of physiology. Cell physiology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
1.6field-weighted citation impact, top 17% 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

15 citing papers in PubMed, 26 citations in OpenAlex.

  1. Article
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  4. Effects of acute and chronic nicotine on catecholamine neurons of the nucleus of the solitary tract.American journal of physiology. Regulatory, integrative and comparative physiology · 2019
    Article
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  9. Presynaptic T-type Ca2+ channels modulate dendrodendritic mitral-mitral and mitral-periglomerular connections in mouse olfactory bulb.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2014
    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

5 authors at 2 institutions in 1 country.

Bopanna I KalappaDepartment of Pharmacology, Southern Illinois University School of Medicine, Springfield, IL 62702, USA.
Lin Feng
William R Kem
Alexander G Gusev
Victor V Uteshev
Southern Illinois University School of Medicine · USUniversity of Florida · US

Funding

Responsiveness to nicotine of nucleus tractus solitarius neuronsR01DK082625 · NIDDK · UNIVERSITY OF NORTH TEXAS HLTH SCI CTR · PI UTESHEV, VICTOR V · 2009 to 2013
$1.7M
Studying nicotinic AChRs in histaminergic neuronsR21DA021216 · NIDA · SOUTHERN ILLINOIS UNIVERSITY CARBONDALE · PI UTESHEV-GAARD, VICTOR V · 2006 to 2007
$341k
NIDA NIH HHS DA021216NIDA NIH HHS R21 DA021216NIDDK NIH HHS DK082625NIDDK NIH HHS R01 DK082625
6 · The paper itself

Abstract

The nucleus of the solitary tract (NTS) is the principal integrating relay in the processing of visceral sensory information. Functional nicotinic acetylcholine receptors (nAChRs) have been found on presynaptic glutamatergic terminals in subsets of caudal NTS neurons. Activation of these receptors has been shown to enhance synaptic release of glutamate and thus may modulate autonomic sensory-motor integration and visceral reflexes. However, the mechanisms of nAChR-mediated facilitation of synaptic glutamate release in the caudal NTS remain elusive. This study uses rat horizontal brainstem slices, patch-clamp electrophysiology, and fluorescent Ca(2+) imaging to test the hypothesis that a direct Ca(2+) entrance into glutamatergic terminals through active presynaptic non-α7- or α7-nAChR-mediated ion channels is sufficient to trigger synaptic glutamate release in subsets of caudal NTS neurons. The results of this study demonstrate that, in the continuous presence of 0.3 μM tetrodotoxin, a selective blocker of voltage-activated Na(+) ion channels, facilitation of synaptic glutamate release by activation of presynaptic nAChRs (detected as an increase in the frequency of miniature excitatory postsynaptic currents) requires external Ca(2+) but does not require activation of presynaptic Ca(2+) stores and presynaptic high- and low-threshold voltage-activated Ca(2+) ion channels. Expanding the knowledge of mechanisms and pharmacology of nAChRs in the caudal NTS should benefit therapeutic approaches aimed at restoring impaired autonomic homeostasis.

Indexed as

alpha7 Nicotinic Acetylcholine ReceptorAnimalsCaffeineCalcium SignalingExcitatory Postsynaptic PotentialsGlutamic AcidIn Vitro TechniquesMecamylamineMicroscopy, FluorescenceNicotineNicotinic AgonistsNicotinic AntagonistsPatch-Clamp TechniquesPresynaptic TerminalsRatsRats, Sprague-Dawleyalpha7 Nicotinic Acetylcholine ReceptorCaffeineChrna7 protein, ratGlutamic AcidMecamylamineNicotineNicotinic AgonistsNicotinic AntagonistsReceptors, NicotinicSodium Channel BlockersTetrodotoxin

Identifiers

PMID21613611
PMCPMC3154558
OpenAlexW2157297172

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.