Acute Postural Effects of Spinal Cord Injury : Dual Neural Opioid and Endocrine Non-Opioid Mechanism
Watanabe, Hiroyuki LU ; Lavrov, Igor ; Hallberg, Mathias ; Schouenborg, Jens LU
; Zhang, Mengliang
LU
and Bakalkin, Georgy
(2025)
In Cells
14(13).
- Abstract
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... (More)
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.
(Less)
- author
- Watanabe, Hiroyuki
LU
; Lavrov, Igor
; Hallberg, Mathias
; Schouenborg, Jens
LU
; Zhang, Mengliang
LU
and Bakalkin, Georgy
- organization
- publishing date
- 2025-07
- type
- Contribution to journal
- publication status
- published
- subject
- keywords
- asymmetric postural deficits, endocrine pathway, lateral hemisection, neurohormones, opioid system, spinal cord injury
- in
- Cells
- volume
- 14
- issue
- 13
- article number
- 980
- publisher
- MDPI AG
- external identifiers
-
- scopus:105010592567
- pmid:40643501
- ISSN
- 2073-4409
- DOI
- 10.3390/cells14130980
- language
- English
- LU publication?
- yes
- additional info
- Publisher Copyright: © 2025 by the authors.
- id
- 1d1ec664-f20c-4eac-808c-e96218c4e604
- date added to LUP
- 2025-12-11 14:44:18
- date last changed
- 2025-12-12 03:00:14
@article{1d1ec664-f20c-4eac-808c-e96218c4e604,
abstract = {{<p>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.</p>}},
author = {{Watanabe, Hiroyuki and Lavrov, Igor and Hallberg, Mathias and Schouenborg, Jens and Zhang, Mengliang and Bakalkin, Georgy}},
issn = {{2073-4409}},
keywords = {{asymmetric postural deficits; endocrine pathway; lateral hemisection; neurohormones; opioid system; spinal cord injury}},
language = {{eng}},
number = {{13}},
publisher = {{MDPI AG}},
series = {{Cells}},
title = {{Acute Postural Effects of Spinal Cord Injury : Dual Neural Opioid and Endocrine Non-Opioid Mechanism}},
url = {{http://dx.doi.org/10.3390/cells14130980}},
doi = {{10.3390/cells14130980}},
volume = {{14}},
year = {{2025}},
}