ArticleThe Journal of biological chemistry2014
Brain-derived neurotrophic factor (BDNF) induces sustained intracellular Ca2+ elevation through the up-regulation of surface transient receptor potential 3 (TRPC3) channels in rodent microglia.
Article in The Journal of biological chemistry, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.
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Who cites it
44 citing papers in PubMed, 78 citations in OpenAlex.
- Calcium signaling in microglial immune functions: current understanding and implications for disease.Current opinion in immunology · 2026Review
- Brain-derived neurotrophic factor via TRPM2 inhibition reduces amyloid-beta-mediated increases of apoptosis and mitochondrial oxidative neurotoxicity in neuronal cells.Metabolic brain disease · 2026Article
- Bidirectional crosstalk between TRP channels and Toll-like receptors in inflammation and host defense.Journal of neuroinflammation · 2026Review
- Synaptic-like coupling of macrophages to myofibers regulates muscle repair.Current biology : CB · 2025Article
- Electrical Stimulation of Cells: Drivers, Technology, and Effects.Chemical reviews · 2025Review
- Spinal TRPC3 promotes neuropathic pain and coordinates phospholipase C-induced mechanical hypersensitivity.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Article
- TRP Channels in Stroke.Neuroscience bulletin · 2024Review
- K252a Prevents Microglial Activation Induced by Anoxic Stimulation of Carotid Bodies in Rats.Toxics · 2023Article
- Urokinase-Type Plasminogen Activator Enhances the Neuroprotective Activity of Brain-Derived Neurotrophic Factor in a Model of Intracerebral Hemorrhage.Biomedicines · 2022Article
- Nitric Oxide Signaling Pathway in Ventral Tegmental Area is Involved in Regulation of 7,8-Dihydroxyflavone on Alcohol Consumption in Rats.Molecular neurobiology · 2022Article
- Preparation of aripiprazole-poly(methyl vinyl ether-Regenerative biomaterials · 2022Article
- Roles of Microglial Ion Channel in Neurodegenerative Diseases.Journal of clinical medicine · 2021Review
- Effect of memantine, an anti-Alzheimer's drug, on rodent microglial cells in vitro.Scientific reports · 2021Article
- Ion channels and transporters in microglial function in physiology and brain diseases.Neurochemistry international · 2021Review
- Microglia Function on Precursor Cells in the Adult Hippocampus and Their Responsiveness to Serotonin Signaling.Frontiers in cell and developmental biology · 2021Review
- The Role of TRP Channels and PMCA in Brain Disorders: Intracellular Calcium and pH Homeostasis.Frontiers in cell and developmental biology · 2021Review
- 14,15-Epoxyeicosatrienoic Acid Alleviates Pathology in a Mouse Model of Alzheimer's Disease.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2020Article
- BDNF reverses aging-related microglial activation.Journal of neuroinflammation · 2020Article
- RNA-seq analysis reveals TRPC genes to impact an unexpected number of metabolic and regulatory pathways.Scientific reports · 2020Article
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Authors and funding
12 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Microglia are immune cells that release factors, including proinflammatory cytokines, nitric oxide (NO), and neurotrophins, following activation after disturbance in the brain. Elevation of intracellular Ca(2+) concentration ([Ca(2+)]i) is important for microglial functions such as the release of cytokines and NO from activated microglia. There is increasing evidence suggesting that pathophysiology of neuropsychiatric disorders is related to the inflammatory responses mediated by microglia. Brain-derived neurotrophic factor (BDNF) is a neurotrophin well known for its roles in the activation of microglia as well as in pathophysiology and/or treatment of neuropsychiatric disorders. In this study, we sought to examine the underlying mechanism of BDNF-induced sustained increase in [Ca(2+)]i in rodent microglial cells. We observed that canonical transient receptor potential 3 (TRPC3) channels contribute to the maintenance of BDNF-induced sustained intracellular Ca(2+) elevation. Immunocytochemical technique and flow cytometry also revealed that BDNF rapidly up-regulated the surface expression of TRPC3 channels in rodent microglial cells. In addition, pretreatment with BDNF suppressed the production of NO induced by tumor necrosis factor α (TNFα), which was prevented by co-adiministration of a selective TRPC3 inhibitor. These suggest that BDNF induces sustained intracellular Ca(2+) elevation through the up-regulation of surface TRPC3 channels and TRPC3 channels could be important for the BDNF-induced suppression of the NO production in activated microglia. We show that TRPC3 channels could also play important roles in microglial functions, which might be important for the regulation of inflammatory responses and may also be involved in the pathophysiology and/or the treatment of neuropsychiatric disorders.
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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.