Evidence map›Paper›PMID 25883550›Full record

ArticleFrontiers in cellular neuroscience2015

Restraint stress increases hemichannel activity in hippocampal glial cells and neurons.

Juan A Orellana, Rodrigo Moraga-Amaro, Raúl Díaz-Galarce, Sebastián Rojas, Carola J Maturana, Jimmy Stehberg, Juan C Sáez

Open access · goldAbstract read
In one paragraph

Article in Frontiers in cellular neuroscience, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 papers.

0numbers the graph read from it
0cells of the map it votes in
56citing papers in PubMed
4.6field-weighted citation impact, top 4% 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

56 citing papers in PubMed, 100 citations in OpenAlex.

  1. Cerebellar astrocytic alterations in depression.Translational psychiatry · 2026
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  5. The role of astrocytes in depression, its prevention, and treatment by targeting astroglial gliotransmitter release.Proceedings of the National Academy of Sciences of the United States of America · 2024
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  6. Article
  7. Review
  8. Article
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  11. Cx43 Hemichannel and Panx1 Channel Modulation by Gap19 andInternational journal of molecular sciences · 2023
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  13. Review
  14. Review
  15. 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

7 authors at 3 institutions in 1 country.

Juan A OrellanaDepartamento de Neurología, Escuela de Medicina, Pontificia Universidad Católica de Chile Santiago, Chile.
Rodrigo Moraga-AmaroLaboratorio de Neurobiología, Centro de Investigaciones Biomédicas, Facultad de Ciencias Biológicas and Facultad de Medicina, Universidad Andres Bello Santiago, Chile.
Raúl Díaz-GalarceLaboratorio de Neurobiología, Centro de Investigaciones Biomédicas, Facultad de Ciencias Biológicas and Facultad de Medicina, Universidad Andres Bello Santiago, Chile.
Sebastián RojasLaboratorio de Neurobiología, Centro de Investigaciones Biomédicas, Facultad de Ciencias Biológicas and Facultad de Medicina, Universidad Andres Bello Santiago, Chile.
Carola J MaturanaDepartamento de Fisiología, Facultad de Ciencias Biológicas, Pontificia Universidad Católica de Chile Santiago, Chile.
Jimmy StehbergLaboratorio de Neurobiología, Centro de Investigaciones Biomédicas, Facultad de Ciencias Biológicas and Facultad de Medicina, Universidad Andres Bello Santiago, Chile.
Juan C SáezDepartamento de Fisiología, Facultad de Ciencias Biológicas, Pontificia Universidad Católica de Chile Santiago, Chile ; Instituto Milenio, Centro Interdisciplinario de Neurociencias de Valparaíso Santiago, Chile.
Universidad Andrés Bello · CLPontificia Universidad Católica de Chile · CLInstituto de Neurociencia Biomédica · CL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Stress affects brain areas involved in learning and emotional responses, which may contribute in the development of cognitive deficits associated with major depression. These effects have been linked to glial cell activation, glutamate release and changes in neuronal plasticity and survival including atrophy of hippocampal apical dendrites, loss of synapses and neuronal death. Under neuro-inflammatory conditions, we recently unveiled a sequential activation of glial cells that release ATP and glutamate via hemichannels inducing neuronal death due to activation of neuronal NMDA/P2X7 receptors and pannexin1 hemichannels. In the present work, we studied if stress-induced glia activation is associated to changes in hemichannel activity. To this end, we compared hemichannel activity of brain cells after acute or chronic restraint stress in mice. Dye uptake experiments in hippocampal slices revealed that acute stress induces opening of both Cx43 and Panx1 hemichannels in astrocytes, which were further increased by chronic stress; whereas enhanced Panx1 hemichannel activity was detected in microglia and neurons after acute/chronic and chronic stress, respectively. Moreover, inhibition of NMDA/P2X7 receptors reduced the chronic stress-induced hemichannel opening, whereas blockade of Cx43 and Panx1 hemichannels fully reduced ATP and glutamate release in hippocampal slices from stressed mice. Thus, we propose that gliotransmitter release through hemichannels may participate in the pathogenesis of stress-associated psychiatric disorders and possibly depression.

Indexed as

connexinsgliahemichannelshippocampusneuronpannexinsstress

Identifiers

PMID25883550
PMCPMC4382970
OpenAlexW2085503883

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Registered trials

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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.