Figure 2.

Microglial upregulation of P2X₄ gene expression induced by PNI is still present in P2X₄-deficient mice. A, In P2X₄^−/− mice, PNI induced β-galactosidase expression in the spinal cord ipsilateral to the lesion whereas no expression was detected in sham animals. Top row, β-Galactosidase immunoreactivity in spinal cord; bottom row: LacZ staining in the dorsal horn (scale bar, 500 μm). B, Post-PNI, ß-galactosidase immunoreactivity (red) colocalized with the microglial marker Iba1 (green). Scale bar, 500 μm. C, P2X₄-gene deletion did not affect P2X₇ expression and function in microglia. Western blot of P2X₇ expression (left) and ATP (1 mm) induced YOPRO uptake in primary microglial culture from wild-type and P2X₄^−/− mice (right). Representative experiment of 3 showing mean fluorescence intensity of all recorded cells (>50) after background substraction.