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Abstract Title:

Prenatal stress causes dendritic atrophy of pyramidal neurons in hippocampal CA3 region by glutamate in offspring rats.

Abstract Source:

Dev Neurobiol. 2010 Feb ;70(2):114-25. PMID: 19950194

Abstract Author(s):

Ning Jia, Kun Yang, Qinru Sun, Qing Cai, Hui Li, Daxin Cheng, Xiaoli Fan, Zhongliang Zhu

Article Affiliation:

Department of Physiology and Pathophysiology, School of Medicine, Xi'an Jiaotong University, Xi'an, Shaanxi 710061, People's Republic of China.

Abstract:

A substantial number of human epidemiological data, as well as experimental studies, suggest that adverse maternal stress during gestation is involved in abnormal behavior, mental, and cognition disorder in offspring. To explore the effect of prenatal stress (PS) on hippocampal neurons, in this study, we observed the dendritic field of pyramidal neurons in hippocampal CA3, examined the concentration of glutamate (Glu), and detected the expression of synaptotagmin-1 (Syt-1) and N-methyl-D-aspartate receptor 1 (NR1) in hippocampus of juvenile female offspring rats. Pregnant rats were divided into two groups: control group (CON) and PS group. Female offspring rats used were 30-day old. The total length of the apical dendrites of pyramidal neurons in hippocampal CA3 of offspring was significantly shorter in PS than that in CON (p<0.01). The number of branch points of the apical dendrites of pyramidal neurons in hippocampal CA3 of offspring was significantly less in PS (p<0.01). PS offspring had a higher concentration of hippocampal Glu compared with CON (p<0.05). PS offspring displayed increased expression of Syt-1 and decreased NR1 in hippocampus compared with CON (p<0.001 and p<0.01, respectively). The expression of NR1 in different hippocampus subfields of offspring was significantly decreased in PS than that in CON (p<0.05-0.01). This study shows that PS increases the Glu in hippocampus and causes apical dendritic atrophy of pyramidal neurons of hippocampal CA3 in offspring rats. The decline of NR1 in hippocampus may be an adaptive response to the increased Glu.

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Sayer Ji
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