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- W2110280070 abstract "Administration of the DNA-alkylating agent methylazoxymethanol acetate (MAM) on embryonic day 17 (E17) produces behavioral and anatomical brain abnormalities, which model some aspects of schizophrenia. This has lead to the premise that MAM rats are a neurodevelopmental model for schizophrenia. However, the underlying molecular pathways affected in this model have not been elucidated. In this study, we investigated the molecular phenotype of adult MAM rats by focusing on the frontal cortex and hippocampal areas, as these are known to be affected in schizophrenia. Proteomic and metabonomic analyses showed that the MAM treatment on E17 resulted primarily in deficits in hippocampal glutamatergic neurotransmission, as seen in some schizophrenia patients. Most importantly, these results were consistent with our finding of functional deficits in glutamatergic neurotransmission, as identified using electrophysiological recordings. Thus, this study provides the first molecular evidence, combined with functional validation, that the MAM-E17 rat model reproduces hippocampal deficits relevant to the pathology of schizophrenia." @default.
- W2110280070 created "2016-06-24" @default.
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- W2110280070 date "2011-09-28" @default.
- W2110280070 modified "2023-09-25" @default.
- W2110280070 title "The Methylazoxymethanol Acetate (MAM-E17) Rat Model: Molecular and Functional Effects in the Hippocampus" @default.
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- W2110280070 doi "https://doi.org/10.1038/npp.2011.219" @default.
- W2110280070 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/3242314" @default.
- W2110280070 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/21956444" @default.
- W2110280070 hasPublicationYear "2011" @default.
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