Evidence map›Paper›PMID 33060559›Full record

ReviewTranslational psychiatry2020

Environmental regulation of the chloride transporter KCC2: switching inflammation off to switch the GABA on?

Davide Pozzi, Marco Rasile, Irene Corradini, Michela Matteoli

Open access · goldAbstract readReview
In one paragraph

Review in Translational psychiatry, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
3.2field-weighted citation impact, top 7% 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

33 citing papers in PubMed, 50 citations in OpenAlex.

  1. Review
  2. GABACellular and molecular neurobiology · 2026
    Review
  3. Article
  4. Review
  5. Article
  6. Article
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  11. Article
  12. Review
  13. Review
  14. Therapeutic potential for KCC2-targeted neurological diseases.The Japanese dental science review · 2023
    Review
  15. Article
  16. Article
  17. Article
  18. Review
  19. Review
  20. Review
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

4 authors at 1 institution in 1 country.

Davide PozziHumanitas University, Department of Biomedical Science, Via Rita Levi Montalcini 4, Pieve Emanuele, MI, Italy. davide.pozzi@humanitasresearch.it.ORCID 0000-0001-6436-0556
Marco RasileHumanitas University, Department of Biomedical Science, Via Rita Levi Montalcini 4, Pieve Emanuele, MI, Italy.
Irene CorradiniHumanitas Clinical and Research Center - IRCCS, via Manzoni 56, Rozzano, MI, Italy.
Michela MatteoliHumanitas Clinical and Research Center - IRCCS, via Manzoni 56, Rozzano, MI, Italy. michela.matteoli@hunimed.eu.
Humanitas University · IT

Funding

Fondazione Cariplo (Cariplo Foundation) 2017-0886Fondazione Cariplo (Cariplo Foundation) 2019-1973Fondazione Telethon (Telethon Foundation) GGP19226AMinistero dell'Istruzione, dell'Università e della Ricerca (Ministry of Education, University and Research) 2017A9MK4RRegione Lombardia (Region of Lombardy) ID239047
6 · The paper itself

Abstract

Chloride homeostasis, the main determinant factor for the dynamic tuning of GABAergic inhibition during development, has emerged as a key element altered in a wide variety of brain disorders. Accordingly, developmental disorders such as schizophrenia, Autism Spectrum Disorder, Down syndrome, epilepsy, and tuberous sclerosis complex (TSC) have been associated with alterations in the expression of genes codifying for either of the two cotransporters involved in the excitatory-to-inhibitory GABA switch, KCC2 and NKCC1. These alterations can result from environmental insults, including prenatal stress and maternal separation which share, as common molecular denominator, the elevation of pro-inflammatory cytokines. In this review we report and systemize recent research articles indicating that different perinatal environmental perturbations affect the expression of chloride transporters, delaying the developmental switch of GABA signaling, and that inflammatory cytokines, in particular interleukin 1β, may represent a key causal factor for this phenomenon. Based on literature data, we provide therefore a unifying conceptual framework, linking environmental hits with the excitatory-to-inhibitory GABA switch in the context of brain developmental disorders.

Indexed as

gamma-Aminobutyric AcidSymportersChloridesDevelopmental DisabilitiesFemaleHumansInflammationK Cl- CotransportersMaternal DeprivationPregnancyPrenatal Exposure Delayed EffectsChloridesgamma-Aminobutyric AcidK Cl- CotransportersSLC12A5 protein, humanSymporters

Identifiers

PMID33060559
PMCPMC7562743
OpenAlexW3093151643

What OpenQuestion 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 OpenQuestion graph.