Evidence map›Paper›PMID 25263033›Full record

ReviewBritish journal of pharmacology2015

Targeting two-pore domain K(+) channels TREK-1 and TASK-3 for the treatment of depression: a new therapeutic concept.

M Borsotto, J Veyssiere, H Moha Ou Maati, C Devader, J Mazella, C Heurteaux

Open access · bronzeAbstract readReview
In one paragraph

Review in British journal of pharmacology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.

0numbers the graph read from it
0cells of the map it votes in
39citing papers in PubMed
2.4field-weighted citation impact, top 11% 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

39 citing papers in PubMed, 62 citations in OpenAlex.

  1. Structural basis for proton inhibition of the two-pore domain KStructure (London, England : 1993) · 2026
    Article
  2. The potassium channel KNature communications · 2025
    Article
  3. Review
  4. The involvement of KTranslational psychiatry · 2024
    Review
  5. Review
  6. Article
  7. C-type inactivation and proton modulation mechanisms of the TASK3 channel.Proceedings of the National Academy of Sciences of the United States of America · 2024
    Article
  8. The Concise Guide to PHARMACOLOGY 2023/24: Ion channels.British journal of pharmacology · 2023
    Article
  9. Review
  10. Review
  11. Article
  12. Review
  13. Potential of Heterogeneous Compounds as Antidepressants: A Narrative Review.International journal of molecular sciences · 2022
    Review
  14. Review
  15. Non-NMDA Mechanisms of Analgesia in Ketamine Analogs.Frontiers in pain research (Lausanne, Switzerland) · 2022
    Article
  16. Article
  17. Review
  18. Article
  19. Article
  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

6 authors at 3 institutions in 1 country.

M BorsottoInstitut de Pharmacologie Moléculaire et Cellulaire, Centre National de la Recherche Scientifique (CNRS) UMR 7275, Université Nice Sophia Antipolis, Valbonne, France.
J Veyssiere
H Moha Ou Maati
C Devader
J Mazella
C Heurteaux
Centre National de la Recherche Scientifique · FRInstitut de Pharmacologie Moléculaire et Cellulaire · FRInstitut de Génomique Fonctionnelle · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Depression is a disease that is particularly frequent, affecting up to 20% of the population in Western countries. The origins of this pathology involve multiple genes as well as environmental and developmental factors leading to a disorder that remains difficult to treat. Several therapies for depression have been developed and these mainly target monoamine neurotransmitters. However, these treatments are not only associated with numerous adverse effects, but they are also ineffective for more than one-third of patients. Therefore, the need to develop new concepts to treat depression is crucial. Recently, studies using knockout mouse models have provided evidence for a crucial role of two members of the two-pore domain potassium channel (K2P ) family, tandem P-domain weak inward rectifying K(+) (TWIK)-related K(+) channel 1 (TREK-1) and TWIK-related acid-sensitive K(+) channel 3 (TASK-3) in the pathophysiology of depression. It is believed that TREK-1 and TASK-3 antagonists could lead to the development of new antidepressants. Herein, we describe the discovery of spadin, a natural peptide released from the maturation of the neurotensin receptor-3 (also known as sortilin), which specifically blocks the activity of the TREK-1 channel and displays particular antidepressant properties, with a rapid onset of action and the absence of adverse effects. The development of such molecules may open a new era in the field of psychiatry.

Indexed as

AnimalsAntidepressive AgentsDepressionHumansPeptidesPotassium Channel BlockersPotassium Channels, Tandem Pore DomainAntidepressive AgentsKCNK9 protein, humanPeptidesPotassium Channel Blockerspotassium channel protein TREK-1Potassium Channels, Tandem Pore Domainspadin peptide

Identifiers

PMID25263033
PMCPMC4301688
OpenAlexW2123932081

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.