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Open Access Research

The enteric bacterial metabolite propionic acid alters brain and plasma phospholipid molecular species: further development of a rodent model of autism spectrum disorders

Raymond H Thomas1*, Melissa M Meeking1, Jennifer R Mepham1, Lisa Tichenoff1, Fred Possmayer2, Suya Liu3 and Derrick F MacFabe1

Author Affiliations

1 The Kilee Patchell-Evans Autism Research Group, Department of Psychology, University of Western Ontario, London, ON, N6A 5C2, Canada

2 Department of Obstetrics/Gynecology and Biochemistry, University of Western Ontario, London Health Sciences Center, London, ON, Canada

3 Biological Mass Spectrometry Laboratory, Department of Biochemistry, University of Western Ontario, London, ON, Canada

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Journal of Neuroinflammation 2012, 9:153  doi:10.1186/1742-2094-9-153

Published: 2 July 2012

Abstract

Gastrointestinal symptoms and altered blood phospholipid profiles have been reported in patients with autism spectrum disorders (ASD). Most of the phospholipid analyses have been conducted on the fatty acid composition of isolated phospholipid classes following hydrolysis. A paucity of information exists on how the intact phospholipid molecular species are altered in ASD. We applied ESI/MS to determine how brain and blood intact phospholipid species were altered during the induction of ASD-like behaviors in rats following intraventricular infusions with the enteric bacterial metabolite propionic acid. Animals were infused daily for 8 days, locomotor activity assessed, and animals killed during the induced behaviors. Propionic acid infusions increased locomotor activity. Lipid analysis revealed treatment altered 21 brain and 30 blood phospholipid molecular species. Notable alterations were observed in the composition of brain SM, diacyl mono and polyunsaturated PC, PI, PS, PE, and plasmalogen PC and PE molecular species. These alterations suggest that the propionic acid rat model is a useful tool to study aberrations in lipid metabolism known to affect membrane fluidity, peroxisomal function, gap junction coupling capacity, signaling, and neuroinflammation, all of which may be associated with the pathogenesis of ASD.

Keywords:
Locomotor activity; Membrane fluidity; Gap junction; Plasmalogens; Docosahexaenoic acid; Oxidative stress