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Partial Sciatic Nerve Ligation: A Mouse Model of Chronic Neuropathic Pain to Study the Antinociceptive Effect of Novel Therapies
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Injecting NMDA and Ro 25-6981 in insular cortex induce neuroplastic changes and neuropathic pain-like behaviour
M S Yoon1,2, C S Koh1, J Lee1,2
1Department of Neurosurgery, Yonsei University College of Medicine, Seoul, South Korea.
European Journal of Pain (London, England)
|June 5, 2018
Summary
A novel animal model, the circuit plasticity reconstruction (CPR) model, successfully mimics neuropathic pain by inducing neuroplastic changes and central sensitization in rats. This model aids in understanding pain mechanisms and developing new therapies.
Area of Science:
- Neuroscience
- Pain Research
- Animal Models
Background:
- Neuropathic pain involves central nervous system hypersensitivity.
- Neuroplastic changes in pain circuitry are implicated in neuropathic pain.
- Existing animal models struggle to investigate these neuroplastic phenomena.
Purpose of the Study:
- To develop a novel animal model, the circuit plasticity reconstruction (CPR) model.
- To mimic central sensitization associated with neuroplastic changes in neuropathic pain.
- To provide a tool for investigating pain mechanisms and therapeutic strategies.
Main Methods:
- Developed the CPR model in Sprague-Dawley rats.
- Injected NMDA and Ro 25-6981 into the insular cortex.
- Applied electrical stimulation to the hind paw and assessed mechanical allodynia using the von Frey test.
- Confirmed neuroplastic changes via PSA-NCAM-positive immunostaining.
Main Results:
- The CPR model induced mechanical allodynia in the left hind paw, persisting for 21 days.
- A modified CPR model without electrical stimulation did not induce allodynia.
- PSA-NCAM immunostaining confirmed neuroplastic changes in the insular cortex of CPR model rats.
Conclusions:
- The CPR model effectively replicates neuroplasticity and central sensitization observed in neuropathic pain.
- This model facilitates the study of mechanisms underlying pain and the development of targeted therapies.
- Findings highlight the role of neuroplasticity in the insular cortex in neuropathic pain development.
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