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Updated: Jan 27, 2026
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Visualizing Clathrin-mediated Endocytosis of G Protein-coupled Receptors at Single-event Resolution via TIRF Microscopy
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G Protein-Coupled Receptor 32 Contributes to Inflammation Resolution and Neuronal Excitability Dysfunction in
Kaixuan Huang1, Jie Li1, Zeng He1
1Epilepsy Research Center of PLA, Department of Neurosurgery, Xinqiao Hospital, Army Medical University (Third Military Medical University), Chongqing, China.
Neuropathology and Applied Neurobiology
|January 26, 2026
Summary
G-protein-coupled receptor 32 (GPR32) is lower in focal cortical dysplasia IIb (FCDIIb) and tuberous sclerosis complex (TSC) lesions, correlating with seizures. Restoring GPR32 may help control epilepsy in these patients.
Area of Science:
- Neuroscience
- Immunology
- Molecular Biology
Background:
- Focal cortical dysplasia IIb (FCDIIb) and tuberous sclerosis complex (TSC) are linked to persistent neuroinflammation, exacerbating epilepsy.
- Current anti-inflammatory mechanisms appear insufficient to resolve neuronal hyperexcitability in these conditions.
Purpose of the Study:
- To investigate the expression and function of G-protein-coupled receptor 32 (GPR32) in the cortical lesions of FCDIIb and TSC patients.
- To determine the role of GPR32 in microglial activation, inflammation, and neuronal excitability.
Main Methods:
- Examined GPR32 expression and distribution in FCDIIb and TSC patient cortical lesions.
- Assessed the impact of GPR32 on human microglial cell activation and inflammatory mediator production.
- Evaluated GPR32's effects on neuronal electrophysiological properties.
Main Results:
- GPR32 and Resolvin D1 levels were significantly reduced in FCDIIb/TSC lesions, correlating negatively with seizure frequency.
- The GPR32/SHP2/NF-κB pathway was downregulated, with GPR32 promoting anti-inflammatory microglial M2 polarization.
- GPR32 reduced neuronal excitability by decreasing spontaneous excitatory postsynaptic current amplitude and frequency.
Conclusions:
- Reduced GPR32 expression is implicated in the epileptogenesis of FCDIIb and TSC.
- GPR32 modulation presents a potential therapeutic strategy for controlling epilepsy in FCDIIb and TSC patients.
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