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Compensatory changes after spinal cord injury in a remyelination deficient mouse model.
Manesh, S B; Kondiles, B R; Wheeler, S; Liu, J; Zhang, L; Chernoff, C; Duncan, G J; Ramer, M S; Tetzlaff, W.
Afiliación
  • Manesh SB; International Collaboration on Repair Discoveries, University of British Columbia, Vancouver, British Columbia, Canada.
  • Kondiles BR; International Collaboration on Repair Discoveries, University of British Columbia, Vancouver, British Columbia, Canada.
  • Wheeler S; Department of Zoology, University of British Columbia, Vancouver, British Columbia, Canada.
  • Liu J; International Collaboration on Repair Discoveries, University of British Columbia, Vancouver, British Columbia, Canada.
  • Zhang L; International Collaboration on Repair Discoveries, University of British Columbia, Vancouver, British Columbia, Canada.
  • Chernoff C; International Collaboration on Repair Discoveries, University of British Columbia, Vancouver, British Columbia, Canada.
  • Duncan GJ; International Collaboration on Repair Discoveries, University of British Columbia, Vancouver, British Columbia, Canada.
  • Ramer MS; International Collaboration on Repair Discoveries, University of British Columbia, Vancouver, British Columbia, Canada.
  • Tetzlaff W; International Collaboration on Repair Discoveries, University of British Columbia, Vancouver, British Columbia, Canada.
J Neurochem ; 2024 Sep 13.
Article en En | MEDLINE | ID: mdl-39268880
ABSTRACT
The development of therapeutic strategies to reduce impairments following spinal cord injury (SCI) motivates an active area of research, because there are no effective therapies. One strategy is to address injury-induced demyelination of spared axons by promoting endogenous or exogenous remyelination. However, previously, we showed that new myelin was not necessary to regain hindlimb stepping following moderate thoracic spinal cord contusion in 3-month-old mice. The present analysis investigated two potential mechanisms by which animals can re-establish locomotion in the absence of remyelination compensation through intact white matter and conduction through spared axons. We induced a severe contusion injury to reduce the spared white matter rim in the remyelination deficient model, with no differences in recovery between remyelination deficient animals and injured littermate controls. We investigated the nodal properties of the axons at the lesion and found that in the remyelination deficient model, axons express the Nav1.2 voltage-gated sodium channel, a sub-type not typically expressed at mature nodes of Ranvier. In a moderate contusion injury, conduction velocities through the lesions of remyelination deficient animals were similar to those in animals with the capacity to remyelinate after injury. Detailed gait analysis and kinematics reveal subtle differences between remyelination deficient animals and remyelination competent controls, but no worse deficits. It is possible that upregulation of Nav1.2 channels may contribute to establishing conduction through the lesion. This conduction could contribute to compensation and regained motor function in mouse models of SCI. Such compensatory mechanism may have implications for interpreting efficacy results for remyelinating interventions in mice and the development of therapies for improving recovery following SCI.
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Idioma: En Revista: J Neurochem Año: 2024 Tipo del documento: Article País de afiliación: Canadá Pais de publicación: Reino Unido
Texto completo
Añadir a Mi BVS
Imprimir
XML
PubMed Links
Buscar en Google

Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Idioma: En Revista: J Neurochem Año: 2024 Tipo del documento: Article País de afiliación: Canadá Pais de publicación: Reino Unido