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Altered brain phospholipid and acylcarnitine profiles in propionic acid infused rodents: further development of a potential model of autism spectrum disorders
Author(s) -
Thomas Raymond H.,
Foley Kelly A.,
Mepham Jennifer R.,
Tichenoff Lisa J.,
Possmayer Fred,
MacFabe Derrick F.
Publication year - 2010
Publication title -
journal of neurochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.75
H-Index - 229
eISSN - 1471-4159
pISSN - 0022-3042
DOI - 10.1111/j.1471-4159.2010.06614.x
Subject(s) - autism , phospholipid , medicine , endocrinology , chemistry , carnitine , fatty acid , metabolite , metabolism , lipid metabolism , butyric acid , phosphatidylethanolamine , autism spectrum disorder , biochemistry , phosphatidylcholine , biology , psychiatry , membrane
J. Neurochem. (2010) 113 , 515–529. Abstract Recent studies have demonstrated intraventricular infusions of propionic acid (PPA) a dietary and enteric short‐chain fatty acid can produce brain and behavioral changes similar to those observed in autism spectrum disorder (ASD). The effects of PPA were further evaluated to determine if there are any alterations in brain lipids associated with the ASD‐like behavioral changes observed following intermittent intraventricular infusions of PPA, the related enteric metabolite butyric acid (BUT) or phosphate‐buffered saline vehicle. Both PPA and BUT produced significant increases ( p < 0.001) in locomotor activity (total distance travelled and stereotypy). PPA and to a lesser extent BUT infusions decreased the levels of total monounsaturates, total ω6 fatty acids, total phosphatidylethanolamine plasmalogens, the ratio of ω6 : ω3 and elevated the levels of total saturates in separated phospholipid species. In addition, total acylcarnitines, total long‐chain (C12–C24) acylcarnitines, total short‐chain (C2 to C9) acylcarnitines, and the ratio of bound to free carnitine were increased following infusions with PPA and BUT. These results provide evidence of a relationship between changes in brain lipid profiles and the occurrence of ASD‐like behaviors using the autism rodent model. We propose that altered brain fatty acid metabolism may contribute to ASD.