Hippocampal neurons plated on poly L lysine coated glass coverslips and after-treatment with the indicated problems, were immunostained using, anti PPARc, anti Tau 1 and anti p JNK antibodies. Nerves were examined using a Zeiss Pascal Confocal microscope, and morphometric studies were performed using Image Pro plus application. we describe the Icotinib clinical trial effect of a few PPARc agonists in neurite and axonal elongation of hippocampal neurons. . We discovered that PPARc activation promotes axon elongation by a procedure that involved JNK activation. Treatment with TZDs notably increased axonal growth and the utilization of PPARc antagonists like GW 9662, canceled axonal elongation induced by TZDs. Neurite outgrowth was not significantly improved by treatment with TZDs, suggesting that PPARc induced effects are specially strong on axonal growth. Pharmacological inhibitors of JNK process stopped TZDs induced axonal elongation, and more importantly, activation of PPARcsignificantly increased JNK activation on hippocampal neurons. Altogether, these results suggest a novel position of PPARc participating in axogenesis and neuronal polarity mediating activation of JNK. These findings extend previous studies that showed a protective function of PPARc in neurodegenerative diseases and confirm a possible use of PPARc activators from the neuronal damage seen in neurodegenerative diseases. Culture media, chemicals and serum were obtained from Sigma, Roche, Digestion Merck, Gibco BRL and Calsein AM from Molecular Probes. . Troglitazone, GW 9662, ciglitazone, and rosiglitazone were obtained from Cayman Chemical. The antibody anti tau 1 was kindly contributed by Dr. Alejandra Alvarez, antibodies, anti PPARc, anti whole JNK, anti p JNK, anti neurofilament, and anti p Extracellular transmission reaction kinase antibodies were from Santa Cruz Biotechnology. 2Sprague Dawley rats used in these experiments were stored at the Faculty of Biological Sciences of the Pontificia Universidad OSI-420 Desmethyl Erlotinib Cato?lica de Chile and handled in accordance with instructions defined and accepted by the Institutional Animal Care and Use Committee at the Faculty of Biological Sciences of the Pontificia Universidad Cato?lica de Chile. 2Hippocampi from Sprague Dawley rats at embryonic day 18 were dissected, and key hippocampal cultures were prepared as previously described. Pregnant dams were anesthetized with CO2 before obtaining the 18-day rat embryos used for the hippocampal cell cultures. All procedures were performed in agreement with the animal handling and bioethical requirements established by Well-being Committee and Institutional Animal Care in the Faculty of Biological Sciences of the Pontificia Universidad Cato?lica de Chile. Hippocampal neurons were seeded in poly L lysine coated wells. Then, cultured hippocampal neurons were treated with RGZ, TGZ, PPARc agonists, and CGZ for 24, 48, and 72 h. Throughout treatment, hippocampal neurons were observed and photographs were taken using video microscopy.