ReviewPsychopharmacology2018
Gap junction channels as potential targets for the treatment of major depressive disorder.
Review in Psychopharmacology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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.
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.
Who cites it
15 citing papers in PubMed, 43 citations in OpenAlex.
- Noncanonical role of astrocytic mitochondrial Cx43: suppressing IDH3α to sustain glycolytic homeostasis against depression.Cell death & disease · 2025Article
- Review
- Neuron-non-neuron electrical coupling networks are involved in chronic stress-induced electrophysiological changes in lateral habenular neurons.The Journal of physiology · 2025Article
- Combining network pharmacology and experimental verification to reveal the mechanism of Chaigui granules in the treatment of depression through PI3K/Akt/mTOR signaling pathways.Metabolic brain disease · 2023Article
- Astroglial Connexin 43-Mediated Gap Junctions and Hemichannels: Potential Antidepressant Mechanisms and the Link to Neuroinflammation.Cellular and molecular neurobiology · 2023Review
- Connexin 43: An Interface Connecting Neuroinflammation to Depression.Molecules (Basel, Switzerland) · 2023Review
- Mahonia Alkaloids (MA) Ameliorate Depression Induced Gap Junction Dysfunction by miR-205/Cx43 Axis.Neurochemical research · 2022Article
- High, in Contrast to Low Levels of Acute Stress Induce Depressive-like Behavior by Involving Astrocytic, in Addition to Microglial P2X7 Receptors in the Rodent Hippocampus.International journal of molecular sciences · 2022Article
- Inhibition of Connexin 36 attenuates HMGB1-mediated depressive-like behaviors induced by chronic unpredictable mild stress.Brain and behavior · 2022Article
- Guanine-Based Purines as an Innovative Target to Treat Major Depressive Disorder.Frontiers in pharmacology · 2021Article
- Mechanism of Chaihu Shugan Powder () for Treating Depression Based on Network Pharmacology.Chinese journal of integrative medicine · 2020Article
- Impaired ATP Release from Brain Astrocytes May be a Cause of Major Depression.Neuroscience bulletin · 2020Article
- Cellular mechanisms and molecular signaling pathways in stress-induced anxiety, depression, and blood-brain barrier inflammation and leakage.Inflammopharmacology · 2020Review
- An Integrative Pharmacology-Based Pattern to Uncover the Pharmacological Mechanism of Ginsenoside H Dripping Pills in the Treatment of Depression.Frontiers in pharmacology · 2020Article
- Pathological ATPergic Signaling in Major Depression and Bipolar Disorder.Frontiers in molecular neuroscience · 2019Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundMajor depressive disorder (MDD) remains a major public health problem worldwide. The association between MDD and the dysfunction of gap junction channels (GJCs) in glial cells, especially astrocytes, is still controversial.
objectiveThis review provides an overview of the role of astrocyte GJCs in LMDD.
resultsExposure to chronic unpredictable stress caused a reduction in connexin expression in the rat prefrontal cortex, a result that is consistent with clinical findings reported in postmortem studies of brains from MDD patients. Chronic antidepressant treatment in these rats increased the expression of connexins. However, pharmacological GJC blockade in normal rodents decreased connexin expression and caused depressive-like behaviors. Furthermore, GJC dysfunction affects electrical conductance, metabolic coupling and secondary messengers, and inflammatory responses, which are consistent with current hypotheses on MDD. All these results provide a comprehensive overview of the neurobiology of MDD.
conclusionThis review supports the hypothesis that the regulation of GJCs between astrocytes could be an underlying mechanism for the therapeutic effect of antidepressants.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.