ERK activation is not involved in the axonal elongation induced by TZDs.

<p>(<b>A</b>) Confocal images from hippocampal neurons that were treated with CGZ (10 µM) for 72 h, in the presence or absence of 5 µM PD 98059 (GW). PD is a specific inhibitor of ERK activation. After treatment, hippocampal neurons were fixed and immunolabeled with anti-tau-1 antibody and photographed in a confocal microscope. (<b>B</b>) Treatment with CGZ plus PD did not significantly affect average axonal length. Data are the mean ± S.E.M. of 3 independent experiments. *<i>p</i><0.05 compared with untreated neurons, **<i>p</i><0.05 compared with neurons treated with PD 98059. Bar = 10 µm. (<b>C</b>) Hippocampal neurons were treated with increasing concentrations of CGZ and GW for 72 h. Cell extracts were prepared for p-ERK and neurofilament (NF) protein levels detection by western blot. A representative blot showed that CGZ increased p-ERK levels with not apparent effect on neurofilament levels. Inhibition of ERK with PD partially prevented the increase of p-ERK induced by CGZ. Data are representative from 3 independent experiments.