Sex-specific programming of offspring emotionality after stress early in pregnancy (J Neurosci, 2008, 28:9055-9065)

報告日期: 2008/12/05
報告時間: 15:10/16:00
報告學生: 葉哲銘
講評老師: 簡伯武

Sex-Specific Programming of Offspring Emotionality after Stress Early in Pregnancy

Bridget R. Mueller and Tracy L. Bale

Department of Animal Biology, School of Veterinary Medicine, University of Pennsylvania, Philadelphia, Pennsylvania 19104

Journal of Neuroscience 28(36):9055–65, 2008


Speaker: Yeh, Che-Ming (葉哲銘)

Commentator: Gean, Po-Wu, Ph.D. (簡伯武 老師) 

Time:15:10~16:00, December 5, 2008

Place: room 602



Recent evidences from animal and human studies suggest that prenatal stress (PS) is associated with neurodevelopmental and mood disorder. PS cause stress-related fetal antecedents express maladaptive behaviors, like anxiety, depression, autism, and schizophrenia. However the mechanism underlying the effect of PS remains unclear. In this study, the authors emphasized that male offspring exposed to stress early in gestation (E-PS) displayed depression like behavior and increased sensitivity to citalopram (a selective serotonin reuptake inhibitor) treatment. They observed E-PS males showed the reduction of SERT (serotonin transporter) in the CA1 and CA2 region of hippocampus, but the expression levels of TPH2, SERT, 5-HT1A on dorsal raphe micropunches were not changed. Detected the alterations in CRF and GR expression, stress-induced responses and DNA methylation were abnormal. This provided important information of epigenetic regulation after stress early in pregnancy. In addition, placenta plays a role in the process of embryo formation. It defenses the harmful molecule or hormone to enter fetal circulatory systems. Analysis of placental gene expression, PPARa (peroxisome proliferator-activated receptor a), IGFBP-1 (insulin-like growth factor binding protein 1), HIF3a (hypoxia-inducible factor 3a), and GLUT4 (glucose transporter 4) dived into two opposing extremes results in male and female placentas. E-PS male placentas showed significant upregulation of PPARa, IGFBP-1, HIF3a, and GLUT4 compared with female. Sex-specific effect of E-PS on adult offspring may contribute to the increased vulnerability to permanent behavioral and neurobiological consequences. In conclusion, the authors indicated that stress experience during early gestation though the regulation of placental epigenetic machinery is critically sex-dependent and behavioral outcome may diverge in males and females.



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