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Pathophysiological and Neurobehavioral Identification of Propionic Acid‐mediated Autism‐mimetic Rat Model
Author(s) -
Lee Seunghoon,
Hong Yonggeun
Publication year - 2015
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.29.1_supplement.lb641
Subject(s) - autism , pathophysiology , proinflammatory cytokine , hippocampus , neurodevelopmental disorder , autism spectrum disorder , medicine , psychology , endocrinology , neuroscience , inflammation , developmental psychology
ASD is a heritable neurodevelopmental disorder with poorly understood and complex etiology. The purpose of this study is to construct autism mimetic animal models, and to establish how to create autism‐mimetic animal models and the standard indicators, through a comparison between the autism clinical aspects, pathophysiological and neurobehavioral alteration. 22 male SD rats were employed and randomly divided the control and propionic acid (500mg/kg) treated rats groups. The rats were subjected behavioral tests, gene expression, and histological analysis for pathophysiological and neurobehavioral alteration. PPA‐treated rats were significantly reduced exploring activity, non‐aggressive behaviors, whereas enhanced aggressive behavior ( ** p<0.01). Proinflammatory cytokine, TNF‐a was continuously upregulated PPA‐treated rats hippocampus following time‐dependent ( ** p<0.01). Expression of GFAP was significantly augmented at day 14 after PPA treatment ( ** p<0.01). In histological evaluation, PPA‐treated rats were significantly reduced diameter of granular cells and thickness of granular cell layer rather than control rats ( ** p<0.01). We suggest that PPA administration could induce a critical role of proinflammatory cytokine elevation and abnormal neural cells organization, which reveal autism‐mimic neurobehaviors, including increment of aggressive behavior, reduction of exploring activity, and exclusive and passive behavior. Funding: 2012R1A1A2005089, 2013R1A2A2A01067169, KGM4611512