ArticleMolecular psychiatry2018
Calhm2 governs astrocytic ATP releasing in the development of depression-like behaviors.
Article in Molecular psychiatry, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 31 papers.
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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.
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Who cites it
31 citing papers in PubMed, 96 citations in OpenAlex.
- Disrupted TFEB/GDNF-cAMP/ATP Coupling Underlies Astrocytic Dysfunction and Depression in LRRK2 G2019S Parkinson's Mice.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Large-Pore Channels at the Maternal-Fetal Interface: Progress and Open Research Avenues.Biology · 2026Review
- From energy metabolism to mood regulation: The rise of lactate as a therapeutic target.Journal of advanced research · 2026Review
- A mechanism of CALHM1 ion channel gating.American journal of physiology. Cell physiology · 2025Article
- MiR-129-5p alleviates depression and anxiety by increasing astrocyte ATP production partly through targeting deubiquitinase Mysm1.PloS one · 2025Article
- Oligomeric rearrangement may regulate channel activity.Biophysics reports · 2024Article
- Article
- Repurposing Ketamine in the Therapy of Depression and Depression-Related Disorders: Recent Advances and Future Potential.Aging and disease · 2024Review
- The neurobiological mechanisms and therapeutic prospect of extracellular ATP in depression.CNS neuroscience & therapeutics · 2024Review
- Quercetin reshapes gut microbiota homeostasis and modulates brain metabolic profile to regulate depression-like behaviors induced by CUMS in rats.Frontiers in pharmacology · 2024Article
- A Review of Research on the Association between Neuron-Astrocyte Signaling Processes and Depressive Symptoms.International journal of molecular sciences · 2023Review
- Deletion of Calhm2 alleviates MPTP-induced Parkinson's disease pathology by inhibiting EFHD2-STAT3 signaling in microglia.Theranostics · 2023Article
- Extracellular ATP/adenosine dynamics in the brain and its role in health and disease.Frontiers in cell and developmental biology · 2023Review
- PRG-1 prevents neonatal stimuli-induced persistent hyperalgesia and memory dysfunction via NSF/Glu/GluR2 signaling.iScience · 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
- P2X2 receptors in pyramidal neurons are critical for regulating vulnerability to chronic stress.Theranostics · 2022Article
- A Possible Causal Involvement of Neuroinflammatory, Purinergic P2X7 Receptors in Psychiatric Disorders.Current neuropharmacology · 2022Article
- Purinergic neurotransmission in the gustatory system.Autonomic neuroscience : basic & clinical · 2021Article
- Astrocytes in depression and Alzheimer's disease.Frontiers of medicine · 2021Review
- APOE4 genotype exacerbates the depression-like behavior of mice during aging through ATP decline.Translational psychiatry · 2021Article
Corrections and comments
- Erratum issuedCalhm2 governs astrocytic ATP releasing in the development of depression-like behaviors.2018 · Jun, M [corrected to Ma, J]; Xiaolong, Q [corrected to Qi, X]; Chaojuan, Y [corrected to Yang, C]; Ruiyuan, P [corrected to Pan, R]; Shukun, W [corrected to Wang, S]; Junbing, W [corrected to Wu, J]; Li, H [corrected to Huang, L]; Hong, C [corrected
Authors and funding
19 authors at 10 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Extracellular ATP is a widespread cell-to-cell signaling molecule in the brain, where it functions as a neuromodulator by activating glia and neurons. Although ATP exerts multiple effects on synaptic plasticity and neuro-glia interactions, as well as in mood disorders, the source and regulation of ATP release remain to be elaborated. Here, we define Calhm2 as an ATP-releasing channel protein based on in vitro and in vivo models. Conventional knockout and conditional astrocyte knockout of Calhm2 both lead to significantly reduced ATP concentrations, loss of hippocampal spine number, neural dysfunction and depression-like behaviors in mice, which can be significantly rescued by ATP replenishment. Our findings identify Calhm2 as a critical ATP-releasing channel that modulates neural activity and as a potential risk factor of depression.
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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.