Neurons of the rat cervical spinal cord express vimentin and neurofilament after intraparenchymal injection of kainic acid
•Some spinal cord perikarya express VIM and NF after experimental injury.•Expression of VIM and NF last for several days after injury.•VIM and NF colocalize in the same perikarya after injury.•VIM and NF expression may be a necessary change to promote recovery of the damaged tissue. Intermediate fil...
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Published in | Neuroscience letters Vol. 643; pp. 103 - 110 |
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Main Authors | , , , , |
Format | Journal Article |
Language | English |
Published |
Ireland
Elsevier B.V
16.03.2017
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Subjects | |
Online Access | Get full text |
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Summary: | •Some spinal cord perikarya express VIM and NF after experimental injury.•Expression of VIM and NF last for several days after injury.•VIM and NF colocalize in the same perikarya after injury.•VIM and NF expression may be a necessary change to promote recovery of the damaged tissue.
Intermediate filaments (IF) can be altered under disorders such as neurodegenerative diseases. Kainic acid (KA) induce behavioral changes and histopathological alterations of the spinal cord of injected rats. Our goal was to evaluate the IF expression in neurons during this injury model. Animals were injected with KA at the C5 segment of the cervical spinal cord and euthanized at 1, 3 and 7 post injection (pi) days. Neuronal cell counting showed a significant loss of neurons at the injection site when compared with those of sham and non-operated animals. Immunohistochemistry for vimentin and neurofilament showed positive labeling of perikarya in sham and KA-injected animals since day 1 pi that lasted for the remaining experimental days. Colocalization analysis between enolase and vimentin or neurofilament confirmed a high index of colocalization in both experimental groups at day 1 pi. This index decreased in sham animals by day 3 pi whereas that of KA-injected animals remained high throughout the experiment. These results may suggest that perikarya initiate an unconventional IF expression, which may respond to the neuronal damage induced by the mechanical injury and the excitotoxic effect of KA. It seems that vimentin and neurofilament expression may be a necessary change to promote recovery of the damaged tissue. |
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Bibliography: | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 |
ISSN: | 0304-3940 1872-7972 |
DOI: | 10.1016/j.neulet.2017.02.029 |