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Long-term Sensory Conflict in Freely Behaving Mice
Published on: February 20, 2019
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CXCL10 Involvement in Vestibular Migraine via the PI3K/AKT Signaling Pathway.
Mao-Mei Song1, Ting-Yan Chen1, Shi-Na Song1
1Department of Neurology, Headache Center, The First Hospital of Shanxi Medical University, Taiyuan, China.
CNS Neuroscience & Therapeutics
|November 18, 2025
Summary
Elevated CXCL10 levels correlate with vestibular migraine (VM) symptom severity. This chemokine activates the PI3K/AKT pathway, driving inflammation and contributing to VM pathogenesis.
Area of Science:
- Neuroscience
- Immunology
- Biochemistry
Background:
- C-X-C motif chemokine ligand 10 (CXCL10) is recognized for its role in pain, particularly neuropathic pain.
- The specific involvement of CXCL10 in the pathophysiology of vestibular migraine (VM) has not been clearly defined.
Purpose of the Study:
- To investigate the association between serum CXCL10 levels and symptom severity in patients with VM.
- To explore the underlying mechanisms of CXCL10 in VM using a rat model, focusing on the PI3K/AKT signaling pathway.
Main Methods:
- Serum CXCL10 levels were measured in VM patients and correlated with headache and dizziness severity.
- In a rat model of VM, the expression of CXCL10, its receptor CXCR3, and components of the PI3K/AKT pathway were analyzed in key brain regions.
- Expression levels of downstream inflammatory factors were also assessed in the rat model.
Main Results:
- VM patients exhibited significantly higher serum CXCL10 levels, which positively correlated with headache and dizziness severity.
- The rat VM model showed increased expression of CXCL10 and CXCR3 in the trigeminal nucleus caudalis and vestibular nuclei.
- Expression of PI3K/AKT pathway molecules and downstream inflammatory factors (IL-1β, IL-6, TNF-α) was significantly elevated in the rat model.
Conclusions:
- CXCL10 plays a significant role in the pathogenesis of VM.
- CXCL10 activates the PI3K/AKT signaling pathway, leading to the release of pro-inflammatory cytokines.
- Targeting CXCL10 or the PI3K/AKT pathway may offer therapeutic strategies for VM.
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