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Friday, May 7, 2010

Treatment with Neuropeptides Attenuates c-fos Expression in a Mouse Model of Fetal Alcohol Syndrome




Fetal alcohol syndrome (FAS) is the most common nongenetic cause of mental retardation and is characterized by neurodevelopmental anomalies. C-fos is a cellular marker of transcriptional activity in the stress-signal pathway. Previously, we showed the treatment with NAP (NAPVSIPQ) + SAL (SALLRSIPA) reversed the learning deficit after prenatal alcohol exposure in FAS.

Our objective was to evaluate if the mechanism of actions of NAP + SAL involves the stress-signal pathway differentiating c-fos expression in mouse brains after prenatal alcohol exposure.

Adult treatment with NAP + SAL restored the down-regulation of c-fos in the hippocampus after prenatal alcohol exposure (p < class="ITALIC">c-fos expression in the cortex.

Adult treatment with NAP + SAL restored the down-regulation of c-fos expression in hippocampus attenuating the alcohol-induced alteration of the stress-signal pathway.


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