ArticleCNS neuroscience & therapeutics2011
Downregulation and upregulation of glial connexins may cause synaptic imbalances responsible for the pathophysiology of bipolar disorder.
Article in CNS neuroscience & therapeutics, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers, 1 of them a synthesis that pooled it.
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Who cites it
9 citing papers in PubMed, 1 synthesis or guideline pooled it, 23 citations in OpenAlex.
- The Dual Role of Connexins in Stroke, Neurotrauma, Neurodegenerative and Psychiatric Disorders: A Global Systematic Review.Molecules (Basel, Switzerland) · 2026Pooled it
- Preliminary exploration of potential biomarkers for heart failure and bipolar disorder: an exploratory study based on bioinformatics.Frontiers in psychiatry · 2025Article
- A Review of Research on the Association between Neuron-Astrocyte Signaling Processes and Depressive Symptoms.International journal of molecular sciences · 2023Review
- Connexin 43: insights into candidate pathological mechanisms of depression and its implications in antidepressant therapy.Acta pharmacologica Sinica · 2022Review
- A Working Hypothesis Regarding Identical Pathomechanisms between Clinical Efficacy and Adverse Reaction of Clozapine via the Activation of Connexin43.International journal of molecular sciences · 2020Review
- Sigma 1 Receptor Antagonists Inhibit Manic-Like Behaviors in Two Congenital Strains of Mice.The international journal of neuropsychopharmacology · 2018Article
- Connexin43- and Pannexin-Based Channels in Neuroinflammation and Cerebral Neuropathies.Frontiers in molecular neuroscience · 2017Review
- Aquaporin-4 knockout exacerbates corticosterone-induced depression by inhibiting astrocyte function and hippocampal neurogenesis.CNS neuroscience & therapeutics · 2014Article
- Glial-specific gene alterations associated with manic behaviors.International journal of bipolar disorders · 2013Article
Corrections and comments
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Authors and funding
1 author at 1 institution in 1 country.
Funding
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Abstract
The model of the pathophysiology of bipolar disorder proposed is based on imbalances in tripartite synapses caused by dysregulations of connexin expression in the astrocytic syncytium. If the expression of connexins is downregulated, a compensatory upregulation of astrocytic receptors may occur and be responsible for the pathophysiology of depression. Conversely, if the expression of connexins is upregulated, the expression of the astrocytic receptors may be downregulated and be responsible for the pathophysiology of mania. In depression, a relative lack of neurotransmitters exerts a protracted synaptic information processing, whereas in mania a relative increase of neurotransmitters may accelerate synaptic information processing. In addition, the modulatory role of gliotransmitters may be affected in bipolar disorder. Since the dysregulations of connexins impair the astrocytic syncytium, these disorders could be explanatory for cognitive impairment both in depression and in mania. Finally, the testability of this model is discussed.
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Registered trials
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