Progressive changes in neurofilament proteins and growth-associated protein-43 immunoreactivities at the site of cervical spinal cord compression in spinal hyperostotic mice.
METHODS
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.


BACKGROUND
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.
Uchida
Kenzo
K
Department of Orthopaedic Surgery, School of Medicine, Fukui Medical University, Matsuoka, Fukui, Japan.
Baba
Hisatoshi
H
Maezawa
Yasuhisa
Y
Kubota
Chikara
C
D000375:Aging / Q000378:metabolism / Q000473:pathology; D000818:Animals; D001369:Axons / Q000378:metabolism / Q000473:pathology; D004195:Disease Models, Animal; D018450:Disease Progression; D019922:GAP-43 Protein / Q000378:metabolism*; D020022:Genetic Predisposition to Disease; D015576:Hyperostosis / Q000150:complications / Q000235:genetics; D007150:Immunohistochemistry; D051379:Mice; D008813:Mice, Inbred ICR; D008815:Mice, Inbred Strains; D009333:Neck; D009413:Nerve Fibers, Myelinated / Q000473:pathology; D016900:Neurofilament Proteins / Q000378:metabolism*; D013116:Spinal Cord / Q000378:metabolism* / Q000473:pathology; D013117:Spinal Cord Compression / Q000209:etiology / Q000378:metabolism* / Q000473:pathology
D019922:GAP-43 Protein; D016900:Neurofilament Proteins