The PPARα Agonist Fenofibrate Reduces Prepulse Inhibition Disruption in a Neurodevelopmental Model of Schizophrenia. (15th May 2012)

• Record Type: Journal Article
• Authors: Rolland, Benjamin; Marche, Kevin; Cottencin, Olivier; Bordet, Régis
• Other Names: Pillai Anilkumar Academic Editor.
• Is Part Of: Schizophrenia research and treatment. Volume 2012(2012)
• Publication Date: 2012-05-15
• Subjects: Schizophrenia -- Periodicals; Schizophrenia; Schizophrenia; Electronic journals; Periodicals; Periodicals; 616.898
• DOI: 10.1155/2012/839853
• Languages: English
• ISSNs: 2090-2085

Abstract

Abstract : Oxidative stress has been implicated in neurodevelopmental theories of schizophrenia. Antioxidant Peroxysome Proliferator-Activated Receptors α (PPAR α ) 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 (P < 0.05 ) in PPIm between groups KN and KF at PND56, which supposes that fenofibrate could be worthy of interest for early neuroprotection in schizophrenia.