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pubmed-article:15252279pubmed:abstractTextWe investigated the cognitive consequences of a prenatal injection of the mitotic inhibitor methylazoxymethanol (MAM) into pregnant rats at embryonic day 15 (E15) or 17 (E17). The male offspring were tested when adult on a version of the radial-arm maze task that assesses spatial working memory with an extended delay, where performance is dependent, in part, on the hippocampal-prefrontal circuit. A major impairment of spatial learning was observed in E15 MAM rats. However, the E17 MAM rats did learn the rule but were impaired selectively in the 30-min delay-interposed task. Morphologically, the E15 MAM rats exhibited dramatic gross brain abnormalities, whereas the E17 MAM animals displayed aberrant cell migration in the hippocampus and a disrupted laminar pattern in the neocortex. These results suggest that late gestational MAM injection (E17) causes a cognitive impairment in a prefrontal cortex-hippocampus-dependent working memory task. This approach could provide a new developmental model of disorders associated with working memory deficits, such as schizophrenia.lld:pubmed
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pubmed-article:15252279pubmed:articleTitleWorking memory deficits in adult rats after prenatal disruption of neurogenesis.lld:pubmed
pubmed-article:15252279pubmed:affiliationINSERM E0117, Hôpital Sainte-Anne, 2 ter rue d'Alésia, Paris, France. gourevitch@chsa.broca.inserm.frlld:pubmed
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