Figure 4

Blocking microglial SK3 channels inhibits p38 MAPK (but not NFκB) activation. Microglia cultures were treated with LPS (100 ng/ml), with or without 100 nM apamin, 5 nM tamapin or 250 pM tamapin. p38 MAPK activation was monitored with a rabbit polyclonal antibody against phosphorylated (active) p38 MAPK (1:50). NF-κB activation was monitored as degradation of IκB-α, using a rabbit polyclonal antibody against IκB-α (1:100). Immunoreactivity was detected using a Cy3-conjugated secondary antibody (1:500). A. The phospho-p38 MAPK fluorescence signal was increased in microglia after 30 min lipopolysaccharide treatment (†p < 0.05). This activation was prevented by 100 nM apamin (*p < 0.05) or 5 nM tamapin (*p < 0.05), but not by 250 pM tamapin. C. NF-κB was activated in microglia after 30 min lipopolysaccharide treatment, as judged by the decrease in IκB-α fluorescence (^†p < 0.05). NF-κB activation was not affected by apamin or tamapin.