Evidence map›Paper›PMID 21129447›Full record

ArticleNeuroscience2011

Heterosynaptic crosstalk: GABA-glutamate metabotropic receptors interactively control glutamate release in solitary tract nucleus.

L G Fernandes, Y-H Jin, M C Andresen

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 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
0.9field-weighted citation impact, top 30% 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

18 citing papers in PubMed, 22 citations in OpenAlex.

  1. Article
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  5. Glutamatergic plasticity within neurocircuits of the dorsal vagal complex and the regulation of gastric functions.American journal of physiology. Gastrointestinal and liver physiology · 2021
    Review
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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 1 institution in 1 country.

L G FernandesDepartment of Physiology and Pharmacology, Oregon Health and Science University, Portland, OR 97239-3098, USA.
Y-H Jin
M C Andresen
Oregon Health & Science University · US

Funding

Transmission Across the First Synapse of the BaroreflexR01HL041119 · NHLBI · UNIVERSITY OF TEXAS MEDICAL BR GALVESTON · PI ANDRESEN, MICHAEL CHRISTIAN · 1991 to 2009
$2.9M
Central TRPV1 in Cardiovascular RegulationR01HL105703 · NHLBI · OREGON HEALTH & SCIENCE UNIVERSITY · PI ANDRESEN, MICHAEL CHRISTIAN · 2011 to 2014
$1.5M
Presynaptic Mechanisms of Neurotransmission in NTSR01HL083115 · NHLBI · OREGON HEALTH & SCIENCE UNIVERSITY · PI ANDRESEN, MICHAEL CHRISTIAN · 2006 to 2009
$1.4M
NHLBI NIH HHS HL-41119NHLBI NIH HHS HL-83115NHLBI NIH HHS R01 HL041119NHLBI NIH HHS R01 HL083115NHLBI NIH HHS R01 HL105703
6 · The paper itself

Abstract

Synaptic terminals often contain metabotropic receptors that act as autoreceptors to control neurotransmitter release. Less appreciated is the heterosynaptic crossover of glutamate receptors to control GABA release and vice versa GABA receptors which control glutamate release. In the brainstem, activation of solitary tract (ST) afferents releases glutamate onto second-order neurons within the solitary tract nucleus (NTS). Multiple metabotropic receptors are expressed in NTS for glutamate (mGluRs) and for GABA (GABA(B)). The present report identifies mGluR regulation of glutamate release at second and higher order sensory neurons in NTS slices. We found strong inhibition of glutamate release to group II and III mGluR activation on mechanically isolated NTS neurons. However, the same mGluR-selective antagonists paradoxically decreased glutamate release (miniature, mEPSCs) at identified second-order NTS neurons. Unaltered amplitudes were consistent with selective presynaptic mGluR actions. GABA(B) blockade in slices resolved the paradoxical differences and revealed a group II/III mGluR negative feedback of mEPSC frequency similar to isolated neurons. Thus, the balance of glutamate control is tipped by mGluR receptors on GABA terminals resulting in predominating heterosynaptic GABA(B) inhibition of glutamate release. Regulation by mGluR or GABA(B) was not consistently evident in excitatory postsynaptic currents (EPSCs) in higher-order NTS neurons demonstrating metabotropic receptor distinctions in processing at different NTS pathway stages. These cellular localizations may figure importantly in understanding interventions such as brain-penetrant compounds or microinjections. We conclude that afferent glutamate release in NTS produces a coordinate presynaptic activation of co-localized mGluR and GABA(B) feedback on cranial afferent terminals to regulate glutamate release.

Indexed as

AnimalsExcitatory Postsynaptic PotentialsFeedback, Physiologicalgamma-Aminobutyric AcidGlutamic AcidIn Vitro TechniquesMaleMiniature Postsynaptic PotentialsNeuronsPresynaptic TerminalsRatsRats, Sprague-DawleyReceptor Cross-TalkReceptors, GABA-BReceptors, Metabotropic GlutamateSolitary Nucleusgamma-Aminobutyric AcidGlutamic AcidReceptors, GABA-BReceptors, Metabotropic Glutamate

Identifiers

PMID21129447
PMCPMC3020236
OpenAlexW2006702269

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.