Following acute neuronal lesions, metabolic imbalance occurs, the rate of glycolysis increases, and methylglyoxal (MGO) forms, finally leading to metabolic dysfunction and inflammation. The glyoxalase system is the main detoxification system for MGO and is impaired following excitotoxicity and stroke. However, it is not known yet whether alterations of the glyoxalase system are also characteristic for other neuronal damage models. Neuronal damage was induced in organotypic hippocampal slice cultures by transection of perforant pathway (PPT; 5 min to 72 h) and N-methyl-D-aspartate (NMDA; 50 μM for 4 h) or in vivo after controlled cortical impact (CCI) injury (2 h to 14 days). Temporal and spatial changes of glyoxalase I (GLO1) were investigated by Western blot analyses and immunohistochemistry. In immunoblot, the GLO1 protein content was not significantly affected by PPT at all investigated time points. As described previously, NMDA treatment led to a GLO1 increase 24 and 48 h after the lesion, whereas PPT increased GLO1 immunoreactivity within neurons only at 48 h postinjury. Immunohistochemistry of brain tissue subjected to CCI unveiled positive GLO1 immunoreactivity in neurons and astrocytes at 1 and 3 days after injury. Two hours and 14 days after CCI, no GLO1 immunoreactivity was observed. GLO1 protein content changes are associated with excitotoxicity but seemingly not to fiber transection. Cell-specific changes in GLO1 immunoreactivity after different in vitro and in vivo lesion types might be a common phenomenon in the aftermath of neuronal lesions.
Keywords: Controlled cortical impact injury; Excitotoxicity; Glyoxalase; Organotypic hippocampal slice culture; Perforant pathway transection.