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Sexual differences in long‐term effects of prenatal chronic mild stress on anxiety‐like behavior and stress‐induced regional glutamate receptor expression in rat offspring
Author(s) -
Wang Yan,
Ma Yuchao,
Cheng Wenwen,
Jiang Han,
Zhang Xinxin,
Li Min,
Ren Jintao,
Zhang Xiaosong,
Li Xiaobai
Publication year - 2015
Publication title -
international journal of developmental neuroscience
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.761
H-Index - 88
eISSN - 1873-474X
pISSN - 0736-5748
DOI - 10.1016/j.ijdevneu.2015.01.003
Subject(s) - offspring , anxiogenic , prenatal stress , elevated plus maze , amygdala , prefrontal cortex , metabotropic glutamate receptor , glutamate receptor , metabotropic glutamate receptor 5 , endocrinology , hippocampus , medicine , anxiety , psychology , chronic stress , receptor , neuroscience , pregnancy , biology , anxiolytic , psychiatry , cognition , genetics
Severe adverse life events during pregnancy may increase the risk of anxiety disorders in the offspring. Glutamate receptors are neurobiological targets in anxiety disorders. In this study, we investigated the effects of prenatal chronic mild stress (PCMS) on anxiety‐like behavior by using elevated plus maze (EPM), and evaluated the effects of PCMS and/or anxiogenic challenge on glutamate receptors in different brain regions. Our results showed that PCMS increased anxiety‐like behavior in both male and female offspring. Moreover, compared with the male naïve rats, male EPM rats showed a significant reduction of mGluR2/3 in the prefrontal cortex, mGluR1 and mGluR2/3 in the hippocampus, and increments of mGluR5, NR1, NR2B and PSD95 in the amygdala. In contrast, compared with female naïve rats, female EPM rats showed decreased levels of mGluR5 in the hippocampus, and mGluR2/3 and mGluR5 in the prefrontal cortex, and increased levels of NR2B and PSD95 in the amygdala. Furthermore, PCMS seemed not to affect the baseline expression of glutamate receptors in adult offspring, but induced significant alterations of them triggered by anxiogenic challenge with a sex difference. These data strengthen the pathophysiological hypothesis that prenatal stress as a risk factor involves in the development of anxiety disorder in the offspring.