The mechanism of enriched environment repairing the learning and memory impairment in offspring of prenatal stress by regulating the expression of activity-regulated cytoskeletal-associated and insulin-like growth factor-2 in hippocampus

Abstract

Background 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. Methods Rats 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. Results There 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. Conclusions 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 IGF-2 and Arc of offspring rats following maternal chronic stress during pregnancy.

Early environmental enrichment prevents cognitive impairments and developing addictive behaviours in a mouse model of prenatal psychological and physical stress

“…The benefits of EE could be attributed to enhanced cerebral cortex thickness and synaptic arborization, enhanced serotonergic transmission in the frontal lobe, elevated levels of brain‐derived neurotrophic factor (BDNF), and increased hippocampal size (Leger et al, 2015). Contrasting with our results, Liu et al found improved memory from EE intervention in prenatally stressed rats that they attributed to hippocampal expression of activity‐regulated cytoskeletal‐associated protein (Arc) and insulin‐like growth factor‐2 (IGF‐2) (Guan et al, 2021). This could be explained by vastly differing methodology and different types of prenatal stress evaluated.…”

Environmental Enrichment Protects Against Cognition Deficits Caused by Sepsis-Associated Encephalopathy

“…This is likely caused by effects of EE on neuroplastic responses to injury. The finding that an EE can reduce the cognition impairment of SAE is in accord with similar observations in animals with other forms of brain dysfunction [43][44][45][46][47][48]. Healthy environments also afford similar benefits to humans.…”

Enriched Environment Effects on Myelination of the Central Nervous System: Role of Glial Cells

“…Microglia-derived IGF-2 can also prevent TNF α -induced death of mature oligodendrocytes in vitro [ 88 ]. EE can increase the mRNA and protein expression levels of hippocampal IGF-2 in the offspring of prenatal chronically stressed rats [ 89 ]. Microglia express activin-A in demyelinating diseases, which is necessary for myelination after development and injury.…”