Stress enhances expression of calcium‐binding proteins and NMDAR subunit genes in the rat hippocampus

Backgrounds Oxidative stress impairs the function of calcium‐binding proteins and deregulates calcium signaling in living organisms. We have previously explored the overexpression of calcium‐binding protein genes in a reactive oxygen and nitrogen species‐induced in vitro cell model of stress that leads to apoptosis. However, in in vivo models, low levels of stress leads to depressive‐like behavior. Here, we aimed to analyze gene expression of major calcium‐binding proteins (calcineurin, calmodulin, calsyntenin, synaptotagmin, and calreticulin) and N‐methyl‐d‐aspartic acid (NMDA) receptor subunits (glutamate receptor ionotropic [GluN] GluN1, GluN2A, and GluN2B) in the hippocampus of stress‐induced rats. Methods Six‐week‐old male Wistar rats were assigned to two stress induction groups and a control group without stress (n = 6). Stress was induced by using H2O2 (3% in water) or by immobilization (using a sticky mat) over a period of 30 days. Expression of calcium‐binding protein genes in the hippocampus, antioxidant assays, structural alterations in hippocampal neurons, and depressive‐like behavior were determined. Results Expression of genes encoding calcium‐binding proteins calcineurin, calsyntenin, synaptotagmin and NMDA receptor subunit GluN1 was enhanced in both chemical and physical stress‐induced rats compared with control rats (4.25 ± 0.05 vs. 1.03 ± 0.02, p