STUDY DESIGN: Immunohistochemical examination of the expression and localization of neurofilament (NF) proteins and growth-associated protein (GAP)-43 in spinal hyperostotic (twy/twy) mice with progressive compression of the cervical spinal cord. OBJECTIVE: To determine the biologic functions of NF proteins and GAP-43 in the mouse cervical spinal cord during chronic mechanical compression. SUMMARY OF BACKGROUND DATA: The pathologic and repair process in the chronically compressed spinal cord are understood poorly. The present authors hypothesized that there existed an increased expression of NF proteins and GAP-43 in twy/twy mice during the lengthy period of spinal cord compression, which resembles compressive myelopathy. METHODS: The cervical spinal cords of 54 twy mice (aged 8 weeks [n = 18], 14 weeks [n = 18], and 20 weeks [n = 18]) and 18 control animals were examined histologically. Using appropriate antibodies, sections were also stained immunohistochemically for NF proteins and GAP-43. RESULTS: Separation of the myelin sheath from the axon and axonal swelling with deformation were detected in the anterior and lateral funiculi of the spinalcords of 20-week-old twy/twy mice. No such changes were noted in 8-week-old twy mice. In twy/twy mice aged 8 and 14 weeks with mild-to-moderate compression, weak immunoreactivities (mainly in the white matter) for NF proteins and GAP-43 were noted; however, in 20-week-old twy/twy mice, these axons stained strongly positive and immunoreactive swollen axons were present. The relative area of GAP-43 immunoreactive axons gradually increased between 8 and 20 weeks in each column, particularly in the anterior and lateral funiculi in the contralateral side of compression. CONCLUSIONS: The results showed that the expression of NF proteins and GAP-43 in the white matter increased proportionally with the magnitude of spinal cord compression, and indicated the possible involvement of GAP-43 in both axonal degeneration and repair processes in the chronically compressed spinal cord.
STUDY DESIGN: Immunohistochemical examination of the expression and localization of neurofilament (NF) proteins and growth-associated protein (GAP)-43 in spinal hyperostotic (twy/twy) mice with progressive compression of the cervical spinal cord. OBJECTIVE: To determine the biologic functions of NF proteins and GAP-43 in the mouse cervical spinal cord during chronic mechanical compression. SUMMARY OF BACKGROUND DATA: The pathologic and repair process in the chronically compressed spinal cord are understood poorly. The present authors hypothesized that there existed an increased expression of NF proteins and GAP-43 in twy/twy mice during the lengthy period of spinal cord compression, which resembles compressive myelopathy. METHODS: The cervical spinal cords of 54 twy mice (aged 8 weeks [n = 18], 14 weeks [n = 18], and 20 weeks [n = 18]) and 18 control animals were examined histologically. Using appropriate antibodies, sections were also stained immunohistochemically for NF proteins and GAP-43. RESULTS: Separation of the myelin sheath from the axon and axonal swelling with deformation were detected in the anterior and lateral funiculi of the spinalcords of 20-week-old twy/twy mice. No such changes were noted in 8-week-old twy mice. In twy/twy mice aged 8 and 14 weeks with mild-to-moderate compression, weak immunoreactivities (mainly in the white matter) for NF proteins and GAP-43 were noted; however, in 20-week-old twy/twy mice, these axons stained strongly positive and immunoreactive swollen axons were present. The relative area of GAP-43 immunoreactive axons gradually increased between 8 and 20 weeks in each column, particularly in the anterior and lateral funiculi in the contralateral side of compression. CONCLUSIONS: The results showed that the expression of NF proteins and GAP-43 in the white matter increased proportionally with the magnitude of spinal cord compression, and indicated the possible involvement of GAP-43 in both axonal degeneration and repair processes in the chronically compressed spinal cord.
Authors: Hideaki Nakajima; Kenzo Uchida; Alexander Rodriguez Guerrero; Shuji Watanabe; Daisuke Sugita; Naoto Takeura; Ai Yoshida; Guang Long; Karina T Wright; William E B Johnson; Hisatoshi Baba Journal: J Neurotrauma Date: 2012-04-18 Impact factor: 5.269