4.7 Article

SRμCT Reveals 3D Microstructural Alterations of the Vascular and Neuronal Network in a Rat Model of Chronic Compressive Thoracic Spinal Cord Injury

期刊

AGING AND DISEASE
卷 11, 期 3, 页码 603-617

出版社

INT SOC AGING & DISEASE
DOI: 10.14336/AD.2019.0529

关键词

chronic spinal cord injury; neurovascular unit; spinal cord microvasculature; SR mu CT; 3D

资金

  1. National Natural Science Foundation of China [81874004, 81672174, 81301522, 81371956, 81301542, 81502331]
  2. Fundamental Research Funds for the Central Universities of Central South University [201 8zzts254]
  3. Science Foundation of Xiangya Hospital for Young Scholar [2017Q1]
  4. New Xiangya Talent Project of the Third Xiangya Hosipital of Central South University [JY201510]
  5. Natural Science Foundation of Hunan Province [2016JJ3176, 2019JJ50959]

向作者/读者索取更多资源

The complex pathology of chronic thoracic spinal cord compression involves vascular and neuroarchitectural repair processes that are still largely unknown. In this study, we used synchrotron radiation microtomography (SR mu CT) to quantitatively characterize the 3D temporal-spatial changes in the vascular and neuronal network after chronic thoracic spinal cord compression in order to obtain further insights into the pathogenesis of this disease and to elucidate its underlying mechanisms. Direct 3D characterization of the spinal cord microvasculature and neural microstructure of the thoracic spinal cord was successfully reconstructed. The significant reduction in vasculature and degeneration of neurons in the thoracic spinal cord visualized via SR mu CT after chronic compression were consistent with the changes detected by immunofluorescence staining. The 3D morphological measurements revealed significant reductions of neurovascular parameters in the thoracic spinal cord after 1 month of compression and became even worse after 6 months without relief of compression. In addition, the distinct 3D morphological twist and the decrease in branches of the central sulcal artery after chronic compression vividly displayed that these could be the potential triggers leading to blood flow reduction and neural deficits of the thoracic spinal cord. Our findings propose a novel methodology for the 3D analysis of neurovascular repair in chronic spinal cord compression, both qualitatively and quantitatively. The results indicated that compression simultaneously caused vascular dysfunction and neuronal network impairment, which should be acknowledged as concurrent events after chronic thoracic spinal cord injury. Combining neuroprotection with vasoprotection may provide promising therapeutic targets for chronic thoracic spinal cord compression.

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