Evidence map›Paper›PMID 26474076›Full record

ArticlePloS one2015

Acidosis-Induced Dysfunction of Cortical GABAergic Neurons through Astrocyte-Related Excitotoxicity.

Li Huang, Shidi Zhao, Wei Lu, Sudong Guan, Yan Zhu, Jin-Hui Wang

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed, 1 pooled it
2.1field-weighted citation impact, top 14% 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

14 citing papers in PubMed, 1 synthesis or guideline pooled it, 32 citations in OpenAlex.

  1. Decreased Brain pH as a Shared Endophenotype of Psychiatric Disorders.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2018
    Pooled it
  2. Article
  3. Article
  4. Review
  5. Article
  6. Acidosis, cognitive dysfunction and motor impairments in patients with kidney disease.Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association · 2021
    Review
  7. Article
  8. Article
  9. Adolescent ΔBiological psychiatry · 2019
    Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. 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

6 authors at 3 institutions in 1 country.

Li HuangDepartment of Pathophysiology, Bengbu Medical College, Bengbu Anhui, China 233000.
Shidi ZhaoDepartment of Pathophysiology, Bengbu Medical College, Bengbu Anhui, China 233000.
Wei LuCollaborative Innovation Center for Neurodegenerative Disorders in Shandong, Qingdao University, Medical College, 38 Dengzhou, Shandong China 266021.
Sudong GuanDepartment of Pathophysiology, Bengbu Medical College, Bengbu Anhui, China 233000.
Yan ZhuDepartment of Pathophysiology, Bengbu Medical College, Bengbu Anhui, China 233000.
Jin-Hui WangInstitute of Biophysics, Chinese Academy of Sciences, Beijing China 100101.
Bengbu Medical College · CNInstitute of Biophysics · CNQingdao University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundAcidosis impairs cognitions and behaviors presumably by acidification-induced changes in neuronal metabolism. Cortical GABAergic neurons are vulnerable to pathological factors and their injury leads to brain dysfunction. How acidosis induces GABAergic neuron injury remains elusive. As the glia cells and neurons interact each other, we intend to examine the role of the astrocytes in acidosis-induced GABAergic neuron injury.

resultsExperiments were done at GABAergic cells and astrocytes in mouse cortical slices. To identify astrocytic involvement in acidosis-induced impairment, we induced the acidification in single GABAergic neuron by infusing proton intracellularly or in both neurons and astrocytes by using proton extracellularly. Compared the effects of intracellular acidification and extracellular acidification on GABAergic neurons, we found that their active intrinsic properties and synaptic outputs appeared more severely impaired in extracellular acidosis than intracellular acidosis. Meanwhile, extracellular acidosis deteriorated glutamate transporter currents on the astrocytes and upregulated excitatory synaptic transmission on the GABAergic neurons. Moreover, the antagonists of glutamate NMDA-/AMPA-receptors partially reverse extracellular acidosis-induced injury in the GABAergic neurons.

conclusionOur studies suggest that acidosis leads to the dysfunction of cortical GABAergic neurons by astrocyte-mediated excitotoxicity, in addition to their metabolic changes as indicated previously.

Indexed as

AcidosisBrain Diseases, MetabolicCerebral CortexGABAergic NeuronsAnimalsMiceMice, TransgenicReceptors, AMPAReceptors, N-Methyl-D-AspartateReceptors, AMPAReceptors, N-Methyl-D-Aspartate

Identifiers

PMID26474076
PMCPMC4608795
OpenAlexW1828091636

What Socratic holds

Textmetadata
LicenceCC BY
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 Socratic graph.