Neurons of the rat cervical spinal cord express vimentin and neurofilament after intraparenchymal injection of kainic acid

NISHIDA F; SISTI MS; ZANUZZI CN; BARBEITO CG; PORTIANSKY EL

Congreso; LXI Reunión anual de la Sociedad Argentina de Investigación Clínica (SAIC), LXIV Reunión anual de la Sociedad Argentina de Inmunología (SAI) y XLVIII Reunión anual de la Sociedad Argentina de Farmacología Experimental (SAFE); 2016

Intermediate filaments are the major components of the cytoskeleton, together with microtubules and microfilaments. Their expression can be altered in neurodegenerative diseases and cancer and, therefore, they can be used as biological markers. Rats injected with Kainic acid (KA) show behavioral changes and histopathological degenerative alterations of their spinal cords. In the present study, we evaluated whether vimentin (VIM) and neurofilament (NF) expression are modified in a KA-induced neurodegenerative rat 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. Immunohistochemistry and double immunofluorescence were carried out for quantification of NeuN, VIM and NF positive cells and to determine colocalization of enolase (NSE)-VIM and NSE-NF. Cell counting of NeuN positive perikarya showed a significant loss of neurons at the injected site (ipsilateral) when compared with those of sham and non-operated animals. The contralateral side remained unchanged in all groups. When the VIM/NeuN positive neurons ratio was calculated in sham animals, a significant reduction was observed at day 7 pi whereas that of NF/NeuN was reduced from day 3 pi. KA-injected rats showed a constant ratio for both markers through the experimental days. Colocalization analysis confirmed a high index of VIM-NSE and NF-NSE in both experimental groups at day 1 pi. This index decreased in sham animals by day 3 pi whereas that of KA-injected rats remained high throughout the experiment. These results suggest that neurons initiate an unconventional intermediate filaments expression, which may respond to both the neuronal damage induced by the mechanical injury and the excitotoxic effect of the KA. The VIM and NF expression here described may function as a relevant molecular tool to reestablish the synaptic connections lost as a result of the neurodegenerative process.