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Indian J Physiol Pharmacol ; 2022 Mar; 66(1): 16-28
Article | IMSEAR | ID: sea-223952

ABSTRACT

Objectives: This study aimed to understand whether an enriched environment (EE) in adulthood benefits in mitigating the early life stress-induced changes in the structure and functions of the hippocampus and amygdala. Materials and Methods: Male Wistar rats were exposed daily for 6 h to early maternal separation and isolation (MS) stress from postnatal days (PND) 4–14 and later at PND 60–70 days subjected to EE, while, the normal control (NC) rats were not subjected to stress but reared with the mother under standard housing conditions. The effects of MS and EE on adulthood behaviour were not subjected to stress but assessed by measuring the ambulatory, repetitive and anxiety-like behaviour. The study has also done the plasma corticosterone concentrations. The dendritic remodelling in the amygdala and hippocampus was assessed using the Golgi cox staining approach. Finally, the present study compared the reactive oxygen species-induced lipid peroxidation and total antioxidant capacity in MS rats as an indirect measure of oxidative stress to study the impact of MS stress on the limbic circuit and peripheral organs. Results: MS rats showed increased anxiety and lower plasma corticosterone levels. The pyramidal neurons’ dendritic plasticity displayed a different pattern, with shrinkage in the CA1 hippocampal neurons and hypertrophy in the amygdala’s primary neurons. Variations in antioxidant activity and peroxidation observed in NC to MS across tissues indicate the occurrence and management of oxidative stress in MS. The 10 days of EE in young adulthood helped to reduce MS stress-induced structural abnormalities in hippocampal and amygdala pyramidal neurons, as well as anxiety and plasma corticosterone levels. Conclusion: These findings together indicate that exposure to adverse experiences may cause harmful effects on brain plasticity and behaviour in young adulthood. Exposure to EE may be beneficial in reducing the early life stress-induced pathophysiology later in life.

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