Aim: 

The AMP-activated protein kinase (AMPK) is a primary sensor of cellular energy change by responding to increases in AMP:ATP ratios. Several conditions, such as hypoxia, glucose deprivation or ischemia, increase AMPK activity through its phosphorylation (p-AMPK). Previous studies have demonstrated that AMPK is involved in the neuroprotection phenomena that follow an ischemic episode. In our previous experiments it has been demonstrated, by RT-PCR, that there is an increase in p-AMPK-1a after cortical spreading depression (CSD), which also can induce tolerance to subsequent episodes of ischemia. The aim of the present work was to evaluate the cell type involved in the expression of pAMPK in the cerebral cortex after CSD.

Methods: 

The expression of pAMPK and GFAP (Glial fibrillary acidic protein) or NeuN (Neuronal Nuclei) has been evaluated by immuonofluorescence in 4 male rats 24h after CSD..

Results: 

The results have shown an increase of pAMPK in the CSD-treated side respect to the contralateral side; the expression of pAMPK was higher in neurons than in glial cells.

Conclusion: 

This result confirm that pAMPK can be involved in the neuroprotection induced by CSD and that its main role is within neuronal cells.