Watanabe Hiroyuki, Lavrov Igor, Hallberg Mathias, Schouenborg Jens, Zhang Mengliang, Bakalkin Georgy
Department of Pharmaceutical Biosciences, Biomedicinskt Centrum BMC, Uppsala University, Husargatan 3, 751 24 Uppsala, Sweden.
Department of Neurology, Mayo Clinic, Rochester, MN 55905, USA.
Cells. 2025 Jun 26;14(13):980. doi: 10.3390/cells14130980.
Lateral spinal cord injury including lateral hemisection (LHS) leads to asymmetric postural and motor deficits. After traumatic brain injury, asymmetric postural deficits are partly developed through activation of opioid receptors. We here characterized the effects of LHS on hindlimb postural asymmetry (HL-PA), a proxy for neurological impairments, and assessed the involvement of opioid system. In acute experiments on rats, high lumbar LHS induced HL-PA, characterized by ipsilateral hindlimb flexion. This asymmetry persisted after complete spinal cord transection at the hemisection level. Treatment with naloxone, a general opioid antagonist, abolished HL-PA both before and after transection, suggesting that the LHS effects are mediated through opioid receptors and that neuroplasticity of lumbar opioid circuits underlies the persistent asymmetry. Surprisingly, cervical LHS performed after complete lumbar spinal cord transection also led to HL-PA. However, the hindlimb was flexed on the contralateral side, and the effect was resistant to naloxone treatment. This asymmetry may be caused by endocrine factors, which convey side-specific messages through the humoral pathway after their release from supraspinal structures. Thus, after lateral spinal cord injury, the asymmetric postural deficits may be driven by an interplay between opposing lumbar opioid and neuroendocrine non-opioid mechanisms.
包括脊髓半切（LHS）在内的脊髓侧方损伤会导致不对称的姿势和运动缺陷。创伤性脑损伤后，不对称姿势缺陷部分是通过阿片受体的激活而形成的。我们在此描述了脊髓侧方损伤对后肢姿势不对称（HL-PA，一种神经功能障碍的指标）的影响，并评估了阿片系统的参与情况。在对大鼠进行的急性实验中，高位腰段脊髓侧方损伤诱发了HL-PA，其特征为同侧后肢屈曲。在半切水平进行完全脊髓横断后，这种不对称仍然存在。使用一般阿片拮抗剂纳洛酮进行治疗，在横断前后均消除了HL-PA，这表明脊髓侧方损伤的影响是通过阿片受体介导的，并且腰段阿片回路的神经可塑性是持续性不对称的基础。令人惊讶的是，在完全腰段脊髓横断后进行的颈段脊髓侧方损伤也导致了HL-PA。然而，后肢在对侧屈曲，并且这种效应对纳洛酮治疗有抵抗性。这种不对称可能是由内分泌因素引起的，这些因素从脊髓上结构释放后通过体液途径传递侧别特异性信息。因此，脊髓侧方损伤后，不对称姿势缺陷可能是由相反的腰段阿片和神经内分泌非阿片机制之间的相互作用驱动的。
