ArticleJournal of neuroinflammation2019
The potassium channel KCa3.1 represents a valid pharmacological target for microgliosis-induced neuronal impairment in a mouse model of Parkinson's disease.
Article in Journal of neuroinflammation, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 42 citations in OpenAlex.
- Mechanistic correlation of potassium channel sensing and nitric oxide activity in neuroinflammation.Molecular biology reports · 2025Review
- Design and structural basis of selective 1,4-dihydropyridine inhibitors of the calcium-activated potassium channel KProceedings of the National Academy of Sciences of the United States of America · 2025Article
- TRPV1 alleviates APOE4-dependent microglial antigen presentation and T cell infiltration in Alzheimer's disease.Translational neurodegeneration · 2024Article
- Controllable mitochondrial aggregation and fusion by a programmable DNA binder.Chemical science · 2023Article
- Non-conducting functions of potassium channels in cancer and neurological disease.Current topics in membranes · 2023Review
- The complex role of inflammation and gliotransmitters in Parkinson's disease.Neurobiology of disease · 2023Review
- A breakdown in microglial metabolic reprogramming causes internalization dysfunction of α-synuclein in a mouse model of Parkinson's disease.Journal of neuroinflammation · 2022Article
- Blocking Intermediate-Conductance Calcium-Activated Potassium Channels in the Macrophages Around Ganglionated Plexi Suppresses Atrial Fibrillation Vulnerability in Canines With Rapid Atrial Pacing.Frontiers in physiology · 2022Article
- Microglial Potassium Channels: From Homeostasis to Neurodegeneration.Biomolecules · 2021Review
- Effect of the KCa3.1 blocker, senicapoc, on cerebral edema and cardiovascular function after cardiac arrest - A randomized experimental rat study.Resuscitation plus · 2021Article
- Treatment with senicapoc in a porcine model of acute respiratory distress syndrome.Intensive care medicine experimental · 2021Article
- A validated UHPLC-MS/MS method for rapid determination of senicapoc in plasma samples.Journal of pharmaceutical and biomedical analysis · 2021Article
- Roles of Microglial Ion Channel in Neurodegenerative Diseases.Journal of clinical medicine · 2021Review
- The Pathogenesis of Parkinson's Disease: A Complex Interplay Between Astrocytes, Microglia, and T Lymphocytes?Frontiers in neurology · 2021Review
- Substantia nigra Smad3 signaling deficiency: relevance to aging and Parkinson's disease and roles of microglia, proinflammatory factors, and MAPK.Journal of neuroinflammation · 2020Article
- Store-Operated Calcium Channels in Physiological and Pathological States of the Nervous System.Frontiers in cellular neuroscience · 2020Review
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundRecent studies described a critical role for microglia in Parkinson's disease (PD), where these central nerve system resident immune cells participate in the neuroinflammatory microenvironment that contributes to dopaminergic neurons loss in the substantia nigra. Understanding the phenotype switch of microgliosis in PD could help to identify the molecular mechanism which could attenuate or delay the progressive decline in motor function. KCa3.1 has been reported to regulate the "pro-inflammatory" phenotype switch of microglia in neurodegenerative pathological conditions.
methodsWe here investigated the effects of gene deletion or pharmacological blockade of KCa3.1 activity in wild-type or KCa3.1
resultsWe report that treatment of MPTP-induced PD mouse model with gene deletion or pharmacological blockade of KCa3.1 with senicapoc improves the locomotor ability and the tyrosine hydroxylase (TH)-positive neuron number and attenuates the microgliosis and neuroinflammation in the substantia nigra pars compacta (SNpc). KCa3.1 involves in store-operated Ca
conclusionsTaken together, these results demonstrate a key role for KCa3.1 in driving a pro-inflammatory microglia phenotype in PD.
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