Evidence map›Paper›PMID 23615553›Full record

ArticleJournal of neurophysiology2013

pH modulation of glial glutamate transporters regulates synaptic transmission in the nucleus of the solitary tract.

Rafiq Huda, Donald R McCrimmon, Marco Martina

Open access · greenAbstract read
In one paragraph

Article in Journal of neurophysiology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
2.0field-weighted citation impact, top 15% 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

20 citing papers in PubMed, 34 citations in OpenAlex.

  1. Article
  2. Review
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  4. The role of astrocytes in the nucleus tractus solitarii in maintaining central control of autonomic function.American journal of physiology. Regulatory, integrative and comparative physiology · 2021
    Review
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  16. Review
  17. PAR1-activated astrocytes in the nucleus of the solitary tract stimulate adjacent neurons via NMDA receptors.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2015
    Article
  18. 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.

Rafiq HudaDepartment of Physiology, Northwestern University Feinberg School of Medicine, Chicago, IL 60611, USA. rafiq.huda@gmail.com
Donald R McCrimmon
Marco Martina
Northwestern University · US

Funding

Central and Peripheral Elements of Respiratory Pattern FormationR01HL088580 · NHLBI · NORTHWESTERN UNIVERSITY AT CHICAGO · PI MC CRIMMON, DONALD R. · 2008 to 2011
$1.5M
Molecular mechanisms of central chemoreception in breathingR01HL095731 · NHLBI · NORTHWESTERN UNIVERSITY AT CHICAGO · PI MARTINA, MARCO · 2010 to 2013
$1.5M
Contribution of ASIC channels to intrinsic chemosensitivity of NTS neuronsF31NS076201 · NINDS · NORTHWESTERN UNIVERSITY AT CHICAGO · PI HUDA, RAFIQ · 2012 to 2013
$53k
NHLBI NIH HHS HL088580NHLBI NIH HHS HL095731NHLBI NIH HHS R01 HL095731NINDS NIH HHS F31 NS076201
6 · The paper itself

Abstract

The nucleus of the solitary tract (NTS) is the major site for termination of visceral sensory afferents contributing to homeostatic regulation of, for example, arterial pressure, gastric motility, and breathing. Whereas much is known about how different neuronal populations influence these functions, information about the role of glia remains scant. In this article, we propose that glia may contribute to NTS functions by modulating excitatory neurotransmission. We found that acidification (pH 7.0) depolarizes NTS glia by inhibiting K(+)-selective membrane currents. NTS glia also showed functional expression of voltage-sensitive glutamate transporters, suggesting that extracellular acidification regulates synaptic transmission by compromising glial glutamate uptake. To test this hypothesis, we evoked glutamatergic slow excitatory potentials (SEPs) in NTS neurons with repetitive stimulation (20 pulses at 10 Hz) of the solitary tract. This SEP depends on accumulation of glutamate following repetitive stimulation, since it was potentiated by blocking glutamate uptake with dl-threo-β-benzyloxyaspartic acid (TBOA) or a glia-specific glutamate transport blocker, dihydrokainate (DHK). Importantly, extracellular acidification (pH 7.0) also potentiated the SEP. This effect appeared to be mediated through a depolarization-induced inhibition of glial transporter activity, because it was occluded by TBOA and DHK. In agreement, pH 7.0 did not directly alter d-aspartate-induced responses in NTS glia or properties of presynaptic glutamate release. Thus acidification-dependent regulation of glial function affects synaptic transmission within the NTS. These results suggest that glia play a modulatory role in the NTS by integrating local tissue signals (such as pH) with synaptic inputs from peripheral afferents.

Indexed as

Amino Acid Transport System X-AGAnimalsHydrogen-Ion ConcentrationIn Vitro TechniquesMaleNeurogliaProtonsRatsRats, Sprague-DawleySolitary NucleusSynaptic TransmissionAmino Acid Transport System X-AGProtonsastrocyteCNS acid-base influencegliaglutamate uptakenucleus of the solitary tractsynaptic transmissionTBOA

Identifiers

PMID23615553
PMCPMC3727073
OpenAlexW2083482752

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.