ORIGINAL RESEARCH article
Front. Pharmacol.
Sec. Neuropharmacology
Volume 16 - 2025 | doi: 10.3389/fphar.2025.1630158
S-ketamine facilitates motor function recovery after brachial plexus root avulsion and reimplantation in mice
Provisionally accepted
Ronghua Huang1
Bingbiao Lin2Lingtai Yu3Qichen Luo4Hongyan Tian4Chenrui Li1
Naili Wei1
Shaohui Zhuang1
Jian Chen1*
Yalan Li4*- 1The First Affiliated Hospital of Shantou University Medical College, Shantou, China
- 2Cancer Hospital of Shantou University Medical College, Shantou, China
- 3The Third Affiliated Hospital, Sun Yat-sen University, Guangzhou, China
- 4First Affiliated Hospital of Jinan University, Guangzhou, China
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Background: Brachial plexus root avulsion (BPRA) often occurs in high-speed traffic accidents or shoulder dystocia, resulting in motor dysfunction. S-ketamine, a clinical anesthetic and antidepressant drug, is an NMDA receptor antagonist that may be effective against glutamate excitotoxicity after nerve injury. Therefore, we aimed to elucidate the potential effectiveness of Sketamine on motor function recovery after BPRA in mice.Methods: A mouse model of BPRA and reimplantation was established and mice were randomly assigned to either the S-ketamine group or the control group, receiving a low and subanesthetic dose of S-ketamine or normal saline respectively. The restoration of the motor neural circuit, from spinal cord, myocutaneous nerve to biceps muscle was evaluated. Fluoro-gold retrograded tracing was utilized to assessed the connectivity between the central and peripheral nerve systems. Behavioral tests such as catwalk, grooming test and grip strength were applied to assess the motor function recovery. The mechanism was analyzed by western blot and rescue experiment was assessed via motor function behavioral tests.Results: S-ketamine increases the motorneuron survival, enhances the central and peripheral nervous connectivity, promote axon regeneration and remyelination, improves the neuromuscular junction integrity and prevents the muscle atrophy. As a result, the motor function recovery was more satisfactory, which was attributed to the advanced BDNF production via ERK-CREB phosphorylation. The BDNF receptor antagonist, ANA12, could counteract the functional recovery of S-ketamine.S-ketamine increases the BDNF concentration via reversing the ERK/CREB phosphorylation, therefore fostering the motor neural circuit repair and facilitating the motor function recovery.
Keywords: S-ketamine, Brachial plexus root avulsion, Motor function, Recovery, BDNF
Received: 17 May 2025; Accepted: 27 Jun 2025.
Copyright: © 2025 Huang, Lin, Yu, Luo, Tian, Li, Wei, Zhuang, Chen and Li. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
* Correspondence:
Jian Chen, The First Affiliated Hospital of Shantou University Medical College, Shantou, China
Yalan Li, First Affiliated Hospital of Jinan University, Guangzhou, China
Disclaimer: All claims expressed in this article are solely those of the authors and do not necessarily represent those of their affiliated organizations, or those of the publisher, the editors and the reviewers. Any product that may be evaluated in this article or claim that may be made by its manufacturer is not guaranteed or endorsed by the publisher.