ArticleFrontiers in molecular neuroscience2019
Pathological ATPergic Signaling in Major Depression and Bipolar Disorder.
Article in Frontiers in molecular neuroscience, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.
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Who cites it
39 citing papers in PubMed, 75 citations in OpenAlex.
- ATP and major affective disorders: the involvement of P2X receptors in pathophysiology.Purinergic signalling · 2026Review
- Establishment and behavioural characterization of a novel constitutive P2X7 receptor knockout mouse line.Purinergic signalling · 2025Article
- P2X7 receptor: a potential target for treating comorbid anxiety and depression.Purinergic signalling · 2025Review
- Review
- Cell Type-Specific Expression of Purinergic P2X Receptors in the Hypothalamus.International journal of molecular sciences · 2025Review
- Purinergic System Transcript Changes in the Dorsolateral Prefrontal Cortex in Suicide and Major Depressive Disorder.International journal of molecular sciences · 2025Article
- Targeting the P2X7 receptor in cerebrovascular diseases: from molecular mechanisms to preclinical therapeutic potential.Frontiers in pharmacology · 2025Review
- Implications of COVID-19 in Parkinson's disease: the purinergic system in a therapeutic-target perspective to diminish neurodegeneration.Purinergic signalling · 2024Review
- P2X7 receptor inhibition alleviates mania-like behavior independently of interleukin-1β.iScience · 2024Article
- Bipolar mania and epilepsy pathophysiology and treatment may converge in purine metabolism: A new perspective on available evidence.Neuropharmacology · 2023Review
- Metabolic features of treatment-refractory major depressive disorder with suicidal ideation.Translational psychiatry · 2023Article
- Role of the P2 × 7 receptor in neurodegenerative diseases and its pharmacological properties.Cell & bioscience · 2023Review
- Electroacupuncture Alleviates Depressive-like Behavior by Modulating the Expression of P2X7/NLRP3/IL-1β of Prefrontal Cortex and Liver in Rats Exposed to Chronic Unpredictable Mild Stress.Brain sciences · 2023Article
- Therapeutic Potential of the Purinergic System in Major Depressive Disorder Associated with COVID-19.Cellular and molecular neurobiology · 2023Review
- Purinergic signaling: a potential therapeutic target for depression and chronic pain.Purinergic signalling · 2023Review
- Microglia in Alzheimer's disease: pathogenesis, mechanisms, and therapeutic potentials.Frontiers in aging neuroscience · 2023Review
- The human P2X7 receptor alters microglial morphology and cytokine secretion following immunomodulation.Frontiers in pharmacology · 2023Article
- Astrocyte regulation of synaptic signaling in psychiatric disorders.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2023Review
- Scrutinizing the Therapeutic Promise of Purinergic Receptors Targeting Depression.Neurotoxicity research · 2022Review
- Beyond Seizure Control: Treating Comorbidities in Epilepsy via Targeting of the P2X7 Receptor.International journal of molecular sciences · 2022Review
Corrections and comments
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Authors and funding
3 authors at 3 institutions in 4 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The mood disorders, major depression (MD) and bipolar disorder (BD), have a high lifetime prevalence in the human population and accordingly generate huge costs for health care. Efficient, rapidly acting, and side-effect-free pharmaceuticals are hitherto not available, and therefore, the identification of new therapeutic targets is an imperative task for (pre)clinical research. Such a target may be the purinergic P2X7 receptor (P2X7R), which is localized in the central nervous system (CNS) at microglial and neuroglial cells mediating neuroinflammation. MD and BD are due to neuroinflammation caused in the first line by the release of the pro-inflammatory cytokine interleukin-1β (IL-1β) from the microglia. IL-1β in turn induces the secretion of corticotropin-releasing hormone (CRH) and in consequence the secretion of adrenocorticotropic hormone (ACTH) and cortisol, which together with a plethora of further cytokines/chemokines lead to mood disorders. A number of biochemical/molecular biological measurements including the use of P2X7R- or IL-1β-deficient mice confirmed this chain of events. More recent studies showed that a decrease in the astrocytic release of ATP in the prefrontal cortex and hippocampus is a major cause of mood disorders. It is an attractive hypothesis that compensatory increases in P2X7Rs in these areas of the brain are the immediate actuators of MD and BD. Hence, blood-brain barrier-permeable P2X7R antagonists may be promising therapeutic tools to improve depressive disorders in humans.
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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.