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Neuron-Microglia Interaction is Involved in Anti-inflammatory Response by Vagus Nerve Stimulation in the Prefrontal
Ki-Joong Kim1, Jinyeon Hwang1, Kang-Woo Lee1
1Department of Korean Medicine, Institute of Bioscience and Integrative Medicine, Daejeon University, Daehak‑ro 62, Daejeon, 34520, South Korea.
Molecular Neurobiology
|February 22, 2024
Summary
Vagus nerve stimulation (VNS) reduced poly(I:C)-induced neuroinflammation and improved mood, memory, and sensory functions in rats. VNS modulated microglial activation and inflammatory markers, highlighting its therapeutic potential for neurological disorders.
Area of Science:
- Neuroscience
- Immunology
- Pharmacology
Background:
- Polyinosinic:polycytidylic acid (poly(I:C)) induces neuroinflammation, modeling anxiety, depression, and fatigue.
- Vagus nerve stimulation (VNS) is explored for its potential to modulate neuroinflammatory processes.
Purpose of the Study:
- To investigate the effects of VNS on poly(I:C)-induced neuroinflammation and associated behavioral changes in rats.
- To elucidate the underlying molecular mechanisms, including microglial activation and inflammatory signaling pathways.
Main Methods:
- Rats were injected with poly(I:C) and treated with acute (aVNS) or chronic (cVNS) VNS.
- Microglial morphology, inflammatory markers (phospho-NF-κB, IL-1β, cleaved caspase 3, phospho-Akt), and fractalkine (CX3CL1) levels were assessed.
- Behavioral tests evaluated pain, depression-like behaviors, and recognition memory.
Main Results:
- aVNS reversed poly(I:C)-induced microglial activation and reduced key inflammatory markers.
- VNS modulated fractalkine-CX3CR1 signaling, suggesting a role in neuron-microglia communication.
- cVNS improved sensory functions, alleviated depressive-like behaviors, and enhanced recognition memory impaired by poly(I:C).
Conclusions:
- VNS demonstrates significant anti-inflammatory effects in the context of poly(I:C)-induced neuroinflammation.
- VNS positively impacts somatosensory, affective, and cognitive functions.
- The fractalkine-CX3CR1 pathway is implicated in VNS-mediated neuroprotection and behavioral improvements.
