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Updated: Mar 2, 2026

Controlled Cortical Impact Model for Traumatic Brain Injury
Published on: August 5, 2014
TRPC Channels and Brain Inflammation
Yoshito Mizoguchi1, Akira Monji2
1Department of Psychiatry, Faculty of Medicine, Saga University, Saga, Japan. ymizo@cc.saga-u.ac.jp.
Abstract:
Nonresolving low-grade inflammation is supposed to underly the basis of chronic disorders including cardiovascular diseases, cancer, diabetes, obesity, and psychiatric disorders such as depression and Alzheimer's diseases. There is increasing evidence suggesting that pathophysiology of psychiatric disorders is related to the inflammatory responses mediated by microglial cells. Elevation of intracellular Ca2+ is important for the activation of microglial cell functions, including proliferation, release of NO, cytokines, and BDNF. It has been shown that alteration of intracellular Ca2+ signaling underlies the pathophysiology of psychiatric disorders, including depression. BDNF induces a sustained intracellular Ca2+ elevation through the upregulation of the surface expression of TRPC3 channels in rodent microglial cells. Microglial cells are able to respond to BDNF, which may be important for the regulation of inflammatory responses and may also be involved in the pathophysiology and/or the treatment of psychiatric disorders. We also need to study the effect of proBDNF on microglial cells especially by focusing on the TRPC channels.
Insights
Chronic inflammation is linked to many diseases. Brain-derived neurotrophic factor (BDNF) affects microglial cells and calcium signaling, potentially impacting psychiatric disorders like depression.
Area of Science:
- Neuroscience
- Immunology
- Cell Biology
Background:
- Nonresolving low-grade inflammation is implicated in chronic diseases, including cardiovascular diseases, cancer, diabetes, obesity, and psychiatric disorders.
- Microglial cells mediate inflammatory responses in the brain, and their activation is linked to the pathophysiology of psychiatric disorders.
- Intracellular calcium (Ca2+) signaling is crucial for microglial cell functions, and its alterations are implicated in psychiatric conditions like depression.
Purpose of the Study:
- To investigate the role of Brain-Derived Neurotrophic Factor (BDNF) in microglial cell activation and calcium signaling.
- To explore the involvement of Transient Receptor Potential Canonical 3 (TRPC3) channels in BDNF-induced microglial responses.
- To understand the potential implications of BDNF-microglial interactions in the context of psychiatric disorders.
Main Methods:
- Utilized rodent microglial cell models.
- Investigated intracellular Ca2+ signaling pathways.
- Examined the expression and function of TRPC3 channels in response to BDNF stimulation.
Main Results:
- BDNF was shown to induce sustained intracellular Ca2+ elevation in microglial cells.
- This effect was mediated by the upregulation of surface expression of TRPC3 channels.
- Microglial cells demonstrate responsiveness to BDNF, suggesting a role in regulating inflammatory responses.
Conclusions:
- BDNF signaling through TRPC3 channels influences microglial cell activity and calcium homeostasis.
- These findings highlight a potential mechanism linking neuroinflammation and psychiatric disorders.
- Further research on proBDNF and TRPC channels in microglial cells is warranted for understanding and treating psychiatric disorders.
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