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Schizophrenia Research and Treatment
Volume 2012 (2012), Article ID 839853, 5 pages
Research Article

The PPAR Agonist Fenofibrate Reduces Prepulse Inhibition Disruption in a Neurodevelopmental Model of Schizophrenia

1Département de Pharmacologie Médicale, EA 1046, Université Lille Nord de France, 1 place de Verdun, 59000 Lille, France
2Service de Psychiatrie et Addictologie, CHU Lille, 59037 Lille, France
3LNFP, EA4559, Université Lille Nord de France, 59000 Lille, France

Received 13 January 2012; Revised 12 March 2012; Accepted 13 March 2012

Academic Editor: Anilkumar Pillai

Copyright © 2012 Benjamin Rolland et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Oxidative stress has been implicated in neurodevelopmental theories of schizophrenia. Antioxidant Peroxysome Proliferator-Activated Receptors α (PPARα) agonist fenofibrate has neuroprotective properties and could reverse early preclinical infringements that could trigger the illness. We have evaluated the neuroprotective interest of fenofibrate in a neurodevelopmental rat model of schizophrenia. The oxidative lesion induced by Kainic Acid (KA) injection at postnatal day (PND) 7 has previously been reported to disrupt Prepulse Inhibition (PPI) at PND56 but not at PND35. In 4 groups of 15 male rats each, KN (KA-PND7 normal postweaning food), KF (KA-PND7 fenofibrate 0.2% food), ON (saline-PND7 normal food), and OF (saline fenofibrate food), PPI was recorded at PND35 and PND56. Three levels of prepulse were used: 73 dB, 76 dB, and 82 dB for a pulse at 120 dB. Four PPI scores were analyzed: PPI73, PPI76, PPI82, and mean PPI (PPIm). Two-way ANOVAs were used to evaluate the effects of both factors (KA fenofibrate), and, in case of significant results, intergroup Student’s t-tests were performed. We notably found a significant difference ( ) in PPIm between groups KN and KF at PND56, which supposes that fenofibrate could be worthy of interest for early neuroprotection in schizophrenia.