Abstract
Background: Selenium (Se) had underscored many bene-ficial neuroprotective potentials, particularly with respect to learning and memory. However, the protective effect of Se in memory impairment associated with Chronic Restraint Stress (CRS) is not yet elucidated.
Aim of Study: The present study was carried out to examine the effect of Se treatment against CRS induced behavioral and biochemical abnormalities.
Material and Methods: The stress was induced by restrain-ing the animals in well ventilated tubes (6h/d) for consecutive 21 days. Animals were randomly divided into 4 groups (8 rats each): Normal control, drug control, CRS and Se treated CRS groups. After 21 days of the experiment, memory function was evaluated by Passive Avoidance (PA), T-maze and object recognition tasks. Hippocampal oxidative stress markers, Brain Derived Neurotrophic Factor (BDNF), amyloid P (AR) protein, phosphorylated TAU (p-TAU) protein as well as glutamate and acetylcholinestrase activity (AchE) levels were assessed.
Results: This study revealed that the memory performance was markedly deteriorated in CRS group, accompanied by noticeable alterations in hippocampal oxidative stress markers, depleted levels of BDNF together with overproduction of AP, p-TAU and glutamate as well as, excessive activity of AchE enzyme. Meanwhile, these behavioral and biochemical devi-ations were alleviated under 21 days of Se co-treatment in CRS exposed rats.
Conclusion: This study proved the beneficial protective effects of Se in CRS-induced memory deficits and its associated pathological changes in rats, which may draw the attention to Se as a new therapeutic candidate for memory dysfunction associated with stress and its related disorders.