Objective: To investigate alterations in the microtubule-associated protein 2 (MAP-2) of neurons in Wistar rats and the effect of nimodipine (Nim), D-2-amino-5-phosphonovaleric acid (D-AP-5) and mild hypothermia on neuronal MAP-2 following fluid percussion injury (FPI).
Methods: Alterations of MAP-2 in Wistar rat neurons following FPI were measured by a confocal laser-scanning microscope using MAP-2 immunofluorescence staining as a MAP-2 indicator.
Results: MAP-2 immunofluorescence staining was limited to the cell bodies and dendritic compartments of neurons and more intense in dendrites than in cell bodies. The loss of MAP-2 was marked at 3 h post-trauma (P < 0.01), and reached a maximum at 48 h post-trauma. Afterwards, fluorescence recovered partly at 72 h post-trauma. The application of Nim markedly reduced the loss of MAP-2 immunoreactivity within 1 h post-trauma (P < 0.01), and the application of D-AP-5 markedly reduced the loss of MAP-2 immunoreactivity within 10 h post-injury (P < 0.01). The application of mild hypothermia decreased the loss of MAP-2 immunoreactivity within 1 h post-injury (P < 0.05).
Conclusions: The partial recovery of fluorescence at 72 h post-trauma indicate that the partial structure of the neuronal microtubules can be repaired by itself. Nim, D-AP-5 and mild hypothermia reduce the degradation of MAP-2 by different mechanisms. The treatment of neuronal cytoskeleton degradation following FPI must employ multiple therapeutic approaches.