Focal traumatic brain injury induces neuroplastic molecular responses in lumbar spinal cord.
Animals
Brain Injuries, Traumatic
/ metabolism
Brain-Derived Neurotrophic Factor
/ metabolism
Disease Models, Animal
GAP-43 Protein
/ metabolism
Gene Expression
Lumbar Vertebrae
Male
Neuronal Plasticity
/ physiology
Neurons
/ metabolism
Proto-Oncogene Proteins c-fos
/ metabolism
RNA, Messenger
/ metabolism
Rats, Sprague-Dawley
Spinal Cord
/ metabolism
Transforming Growth Factor beta1
/ metabolism
Tgfb1
Traumatic brain injury
c-Fos
plasticity
spinal cord
Journal
Restorative neurology and neuroscience
ISSN: 1878-3627
Titre abrégé: Restor Neurol Neurosci
Pays: Netherlands
ID NLM: 9005499
Informations de publication
Date de publication:
2019
2019
Historique:
pubmed:
12
3
2019
medline:
10
7
2019
entrez:
12
3
2019
Statut:
ppublish
Résumé
Motor impairment induced by traumatic brain injury (TBI) may be mediated through changes in spinal molecular systems regulating neuronal plasticity. We assessed whether a focal controlled cortical impact (CCI) TBI in the rat alters expression of the Tgfb1, c-Fos, Bdnf, and Gap43 neuroplasticity genes in lumbar spinal cord.Approach/Methods:Adult male Sprague-Dawley rats (n = 8) were subjected to a right-side CCI over the anterior sensorimotor hindlimb representation area or sham-injury (n = 8). Absolute expression levels of Tgfb1, c-Fos, Bdnf, and Gapd43 genes were measured by droplet digital PCR in ipsi-and contralesional, dorsal and ventral quadrants of the L4 and L5 spinal cord. The neuronal activity marker c-Fos was analysed by immunohistochemistry in the dorsal L4 and L5 segments. The contra- vs. ipsilesional expression pattern was examined as the asymmetry index, AI. The Tgfb1 mRNA levels were significantly higher in the CCI vs. sham-injured rats, and in the contra- vs. ipsilesional dorsal domains in the CCI group. The number of c-Fos-positive cells was elevated in the L4 and L5 segments; and on the contralesional compared to the ipsilesional side in the CCI group. The c-Fos AI in the dorsal laminae was significantly increased by CCI. The results support the hypothesis that focal TBI induces plastic alterations in the lumbar spinal cord that may contribute to either motor recovery or maladaptive motor responses.
Sections du résumé
BACKGROUND/OBJECTIVES
Motor impairment induced by traumatic brain injury (TBI) may be mediated through changes in spinal molecular systems regulating neuronal plasticity. We assessed whether a focal controlled cortical impact (CCI) TBI in the rat alters expression of the Tgfb1, c-Fos, Bdnf, and Gap43 neuroplasticity genes in lumbar spinal cord.Approach/Methods:Adult male Sprague-Dawley rats (n = 8) were subjected to a right-side CCI over the anterior sensorimotor hindlimb representation area or sham-injury (n = 8). Absolute expression levels of Tgfb1, c-Fos, Bdnf, and Gapd43 genes were measured by droplet digital PCR in ipsi-and contralesional, dorsal and ventral quadrants of the L4 and L5 spinal cord. The neuronal activity marker c-Fos was analysed by immunohistochemistry in the dorsal L4 and L5 segments. The contra- vs. ipsilesional expression pattern was examined as the asymmetry index, AI.
RESULTS
The Tgfb1 mRNA levels were significantly higher in the CCI vs. sham-injured rats, and in the contra- vs. ipsilesional dorsal domains in the CCI group. The number of c-Fos-positive cells was elevated in the L4 and L5 segments; and on the contralesional compared to the ipsilesional side in the CCI group. The c-Fos AI in the dorsal laminae was significantly increased by CCI.
CONCLUSIONS
The results support the hypothesis that focal TBI induces plastic alterations in the lumbar spinal cord that may contribute to either motor recovery or maladaptive motor responses.
Identifiants
pubmed: 30856132
pii: RNN180882
doi: 10.3233/RNN-180882
pmc: PMC6484246
doi:
Substances chimiques
Bdnf protein, rat
0
Brain-Derived Neurotrophic Factor
0
GAP-43 Protein
0
Proto-Oncogene Proteins c-fos
0
RNA, Messenger
0
Tgfb1 protein, rat
0
Transforming Growth Factor beta1
0
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
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