Lamotrigine Enhances Autophagy and Reduces Post-Traumatic Spinal Neural Injury in Mice
Background: Lamotrigine (LTG) is an antiepileptic drug that stabilizes the presynaptic membrane by blocking sodium channels and inhibiting excessive glutamate release. Its neuroprotective effects have been demonstrated in various pathological states. However, the role of LTG in sp...
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IMR Press
2025-05-01
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| Series: | Journal of Integrative Neuroscience |
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| Online Access: | https://www.imrpress.com/journal/JIN/24/5/10.31083/JIN37357 |
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| author | Mengting Zhang Li Chen Heren Gao Tao Liu |
| author_facet | Mengting Zhang Li Chen Heren Gao Tao Liu |
| author_sort | Mengting Zhang |
| collection | DOAJ |
| description | Background: Lamotrigine (LTG) is an antiepileptic drug that stabilizes the presynaptic membrane by blocking sodium channels and inhibiting excessive glutamate release. Its neuroprotective effects have been demonstrated in various pathological states. However, the role of LTG in spinal cord injury (SCI) and its relationship with autophagy, which is essential for cellular homeostasis, warrant further investigation. Methods: We established a mouse model of SCI using complete spinal transection. The neuroprotective effects of LTG were assessed using immunostaining and functional assessments, including Basso Mouse Scale (BMS) scores, lesion site area, and synapse survival. Western blot analyses were also performed to further examine the underlying cellular and molecular mechanisms of autophagy. Results: LTG treatment promoted the post-traumatic survival of spinal neurons, improved BMS scores, reduced lesion site area, and enhanced synapse survival in a mouse model of SCI. Furthermore, LTG attenuated apoptosis following SCI by activating autophagy during the secondary injury phase. These findings indicate that LTG-enhanced autophagosome formation and autolysosome degradation play a key role in reducing neuronal loss after SCI. Conclusion: LTG appears to attenuate post-traumatic spinal neural injury by enhancing autophagy flux. |
| format | Article |
| id | doaj-art-2b5463f76c394e1a9b04b3c2d700e5a6 |
| institution | Kabale University |
| issn | 0219-6352 |
| language | English |
| publishDate | 2025-05-01 |
| publisher | IMR Press |
| record_format | Article |
| series | Journal of Integrative Neuroscience |
| spelling | doaj-art-2b5463f76c394e1a9b04b3c2d700e5a62025-08-20T03:25:59ZengIMR PressJournal of Integrative Neuroscience0219-63522025-05-012453735710.31083/JIN37357S0219-6352(25)00929-5Lamotrigine Enhances Autophagy and Reduces Post-Traumatic Spinal Neural Injury in MiceMengting Zhang0Li Chen1Heren Gao2Tao Liu3College of Integrated Chinese and Western Medicine, Anhui University of Chinese Medicine, 230012 Hefei, Anhui, ChinaDepartment of neurology, Shanghai Sixth People’s Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, 201306 Shanghai, ChinaCollege of Acupuncture and Massage, Anhui University of Chinese Medicine, 230012 Hefei, Anhui, ChinaOrthopedic Center, Maanshan General Hospital of Ranger-Duree Healthcare, 243000 Maanshan, Anhui, ChinaBackground: Lamotrigine (LTG) is an antiepileptic drug that stabilizes the presynaptic membrane by blocking sodium channels and inhibiting excessive glutamate release. Its neuroprotective effects have been demonstrated in various pathological states. However, the role of LTG in spinal cord injury (SCI) and its relationship with autophagy, which is essential for cellular homeostasis, warrant further investigation. Methods: We established a mouse model of SCI using complete spinal transection. The neuroprotective effects of LTG were assessed using immunostaining and functional assessments, including Basso Mouse Scale (BMS) scores, lesion site area, and synapse survival. Western blot analyses were also performed to further examine the underlying cellular and molecular mechanisms of autophagy. Results: LTG treatment promoted the post-traumatic survival of spinal neurons, improved BMS scores, reduced lesion site area, and enhanced synapse survival in a mouse model of SCI. Furthermore, LTG attenuated apoptosis following SCI by activating autophagy during the secondary injury phase. These findings indicate that LTG-enhanced autophagosome formation and autolysosome degradation play a key role in reducing neuronal loss after SCI. Conclusion: LTG appears to attenuate post-traumatic spinal neural injury by enhancing autophagy flux.https://www.imrpress.com/journal/JIN/24/5/10.31083/JIN37357lamotrigineautophagyspinal cord injuriesapoptosisneuroprotection |
| spellingShingle | Mengting Zhang Li Chen Heren Gao Tao Liu Lamotrigine Enhances Autophagy and Reduces Post-Traumatic Spinal Neural Injury in Mice Journal of Integrative Neuroscience lamotrigine autophagy spinal cord injuries apoptosis neuroprotection |
| title | Lamotrigine Enhances Autophagy and Reduces Post-Traumatic Spinal Neural Injury in Mice |
| title_full | Lamotrigine Enhances Autophagy and Reduces Post-Traumatic Spinal Neural Injury in Mice |
| title_fullStr | Lamotrigine Enhances Autophagy and Reduces Post-Traumatic Spinal Neural Injury in Mice |
| title_full_unstemmed | Lamotrigine Enhances Autophagy and Reduces Post-Traumatic Spinal Neural Injury in Mice |
| title_short | Lamotrigine Enhances Autophagy and Reduces Post-Traumatic Spinal Neural Injury in Mice |
| title_sort | lamotrigine enhances autophagy and reduces post traumatic spinal neural injury in mice |
| topic | lamotrigine autophagy spinal cord injuries apoptosis neuroprotection |
| url | https://www.imrpress.com/journal/JIN/24/5/10.31083/JIN37357 |
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