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Updated: May 21, 2026
04:39
In-Vivo Calcium Imaging of Sensory Neurons in the Rat Trigeminal Ganglion
Published on: February 9, 2024
Trigeminal nerve injury ErbB3/ErbB2 promotes mechanical hypersensitivity
Fei Ma1, Liping Zhang, Karin N Westlund
1Department of Physiology, University of Kentucky, Lexington, KY, USA.
Anesthesiology
|June 19, 2012
Summary
Neuregulin 1-ErbB3-ErbB2 signaling drives trigeminal neuropathic pain after nerve injury. Inhibiting this pathway with Lapatinib alleviates mechanical allodynia, suggesting a therapeutic target for nerve injury pain.
Area of Science:
- Neuroscience
- Molecular Biology
- Pain Research
Background:
- Chronic constriction injury of the trigeminal infraorbital nerve in rats causes mechanical allodynia.
- Neuregulin 1 (NRG1) interacts with receptor tyrosine kinase ErbB, promoting Schwann cell remyelination.
- This study explored the role of ErbB3-ErbB2 heterodimers in signaling orofacial mechanical allodynia following nerve injury.
Purpose of the Study:
- To investigate the role of Neuregulin 1-ErbB3-ErbB2 signaling in trigeminal neuropathic pain.
- To determine if inhibiting ErbB2 with Lapatinib can alleviate mechanical allodynia after nerve injury.
- To understand the peripheral glial mechanisms involved in nerve injury-induced pain.
Main Methods:
- Quantified mechanical allodynia using von Frey stimuli in wild type and transgenic rats.
- Administered the ErbB2 inhibitor Lapatinib intraperitoneally.
- Evaluated infraorbital nerve injury histologically and measured ErbB3 expression via western blots.
Main Results:
- Mechanical allodynia developed in wild type rats by week 2 but was delayed in transgenic rats.
- Lapatinib treatment significantly alleviated mechanical allodynia in wild type rats.
- Increased ErbB3 expression correlated with the presence of mechanical hypersensitivity in both rat groups.
Conclusions:
- The Neuregulin 1-ErbB3-ErbB2 complex is a key mechanism in trigeminal neuropathic pain following nerve injury.
- Targeting peripheral glial mechanisms, specifically the NRG1-ErbB pathway, holds promise for treating neuropathic pain.
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