Changes in and effective factors of microtubule-associated protein 2 in traumatic neurons

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 measu red 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 an d dendritic compartments of neurons and more intense in dendrites than in c ell bodies. The loss of MAP-2 was marked at 3 h posttrauma (P < 0.01), and reached a maximum at 48 h post-trauma. Afterwards, fluorescence recovered p artly 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 appl ication of D-AP-5 markedly reduced the loss of K4AP-2 immunoreactivity with in 10 h post-injury (P < 0.01). The application of mild hypothermia decreas ed the loss of MAP-2 immunoreactivity within 1 h post-injury ( P <less than > 0.05). Conclusions The partial recovery of fluorescence at 72 h post-trauma indica te 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 degradatio n following FPI must employ multiple therapeutic approaches.