Abstract
BackgroundPrenatal stress can cause neurobiological and behavioral defects in offspring; environmental factors play a crucial role in regulating the development of brain and behavioral; this study was designed to test and verify whether an enriched environment can repair learning and memory impairment in offspring rats induced by prenatal stress and to explore its mechanism involving the expression of insulin-like growth factor-2 (IGF-2) and activity-regulated cytoskeletal-associated protein (Arc) in the hippocampus of the offspring.MethodsRats were selected to establish a chronic unpredictable mild stress (CUMS) model during pregnancy. Offspring were weaned on 21st day and housed under either standard or an enriched environment. The learning and memory ability were tested using Morris water maze and Y-maze. The expression of IGF-2 and Arc mRNA and protein were respectively measured by using RT-PCR and Western blotting.ResultsThere was an elevation in the plasma corticosterone level of rat model of maternal chronic stress during pregnancy. Maternal stress’s offspring exposed to an enriched environment could decrease their plasma corticosterone level and improve their weight. The offspring of maternal stress during pregnancy exhibited abnormalities in Morris water maze and Y-maze, which were improved in an enriched environment. The expression of IGF-2, Arc mRNA, and protein in offspring of maternal stress during pregnancy was boosted and some relationships existed between these parameters after being exposed enriched environment.ConclusionsThe learning and memory impairment in offspring of prenatal stress can be rectified by the enriched environment, the mechanism of which is related to the decreasing plasma corticosterone and increasing hippocampal IGF-2 and Arc of offspring rats following maternal chronic stress during pregnancy.
Highlights
Pregnancy is regarded as an important event during woman’s life
The learning and memory impairment in offspring of prenatal stress can be rectified by the enriched environment, the mechanism of which is related to the decreasing plasma corticosterone and increasing hippocampal insulin-like growth factor-2 (IGF-2) and Activity-regulated cytoskeletalassociated protein (Arc) of offspring rats following maternal chronic stress during pregnancy
Establishment and confirmation of prenatal stress The repeated measurement analysis of variance revealed that chronic stress had a significant impact on the maternal corticosterone level (P = 0.001), and corticosterone level of the PS group obviously changed with stress time (P < 0.001)
Summary
Pregnancy is regarded as an important event during woman’s life. Women are more likely to be exposed to life stress events during pregnancy, including work pressure, family conflicts, economic distress, etc. Numerous studies have demonstrated that the fetal period plays an important role in the development of cognition, behavior, and cognitive function in offspring [2, 3]; this view was called “developmental programming hypothesis,” which was first highlighted by Dr David Barker nearly 30 years [4]. Adverse events during pregnancy can cause neurobiological and behavioral defects in offspring, especially some of which involve the morphological structure and functional disorders of the hippocampus [15]. Prenatal stress can cause neurobiological and behavioral defects in offspring; environmental factors play a crucial role in regulating the development of brain and behavioral; this study was designed to test and verify whether an enriched environment can repair learning and memory impairment in offspring rats induced by prenatal stress and to explore its mechanism involving the expression of insulin-like growth factor-2 (IGF-2) and activity-regulated cytoskeletal-associated protein (Arc) in the hippocampus of the offspring
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