Blockage of PPARγ activation prevented the increase of axonal growth induced by TZDs.

<p>(<b>A</b>) Confocal images from hippocampal neurons that were treated with PPARγactivators: TGZ (10 µM), RGZ (10 µM), and CGZ (10 µM) for 72 h, in the presence or absence of 5 µM GW 4622 (GW). GW is a specific inhibitor of PPARγ activity <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0065140#pone.0065140-Inestrosa1" target="_blank">[11]</a>. After treatment hippocampal neurons were fixed and immunolabeled with anti-tau-1 antibody and then were photographed in a confocal microscope. (<b>B</b>) Quantification of total neurite length on hippocampal neurons exposed to TZDs, in the presence or absence of GW for 72 h. Treatment with PPARγ activators plus GW did not significantly affect total neurite length of hippocampal neurons. Data are the mean ± S.E.M. of 4 independent experiments, *<i>p</i><0.05. (<b>C</b>) Quantification of average axonal length in hippocampal neurons treated with TZDs in the presence or absence of GW for 72 h. Data are the mean ± S.E.M. of 4 independent experiments, *<i>p</i><0.05.