Investigating the role of brivaracetam in pain management: Insights from a vincristine-induced neuropathic pain model in rats
Objectives: Neuropathic pain, characterised by abnormal pain processing, often arises due to nerve injury or chemotherapy-induced neurotoxicity. Current pharmacological interventions, including anticonvulsants and antidepressants, provide partial relief with adverse effects. Brivaracetam (BRV), a synaptic vesicle 2A ligand, has demonstrated neuroprotective effects in preclinical models. This study explores its potential analgesic properties in a vincristine-induced neuropathy model. Materials and Methods: Rats were administered vincristine (0.1 mg/kg, intraperitoneally) for 10 days to induce neuropathy. BRV (10 mg/kg and 20 mg/kg) was administered daily for 14 post-induction. Behavioural assessments, including the von Frey filament test and hot plate test, were performed to evaluate mechanical and thermal hyperalgesia. Results: Vincristine treatment resulted in significant hyperalgesia and nociceptive responses in the control group. BRV-treated rats exhibited significant improvement in pain thresholds compared to the control group ( P < 0.05). This demonstrates the substantial antinociceptive properties. Furthermore, the comparative analysis indicated that BRV provides similar levels of pain relief as gabapentin, supporting its potential utility in pain management. Conclusion: This study demonstrates BRV’s potential in mitigating vincristine-induced neuropathic pain, warranting further clinical investigations. Its multimodal action could offer a novel approach to neuropathic pain treatment.
Authors
- Santhanalakshmi P
- Manimekalai K.
- Vasanth K. S.
Institutions
- Sri Balaji Vidyapeeth University (IN)
- Mahatma Gandhi Medical College and Research Institute (IN)
Publication Details
- Journal
- Indian Journal of Physiology and Pharmacology
- Published
- 2026-03-16
- DOI
- https://doi.org/10.25259/ijpp_480_2024
- Primary Topic
- Pain Mechanisms and Treatments
- Type
- article
- Field-Weighted Citation Impact
- 0.00