الفهرس 
INTRODUCTIONOnly 14 pages are availabe for public view
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Abstract
Exposure to stress on a daily basis has been found to affect the body both physically and psychologically. Stress can be acute or chronic based on its duration. As regard its nature, it can be physical or psychological. The bodily response to stress takes place through two systems: Sympatho-adreno-medullary axis, which is consistent with the rapid stress response and hypothalamic pituitary adreno-cortical axis, which is concerned with the slower and more prolonged stress response.
Exposure to chronic psychological stress leads to overactivation of HPA axis with consequent sustained elevation in the level of glucocorticoids, which in turn induces structural and functional changes in the brain, specifically the prefrontal cortex, hippocampus and amygdala. Many studies demonstrated that chronic psychological stress decreased the level of many brain neurotransmitters and induces neuronal oxidative stress, neuroinflammation and neuronal apoptosis. chronic restraint stress animal model proved to mimic the consequences of chronic psychological stress in humans.
Selenium nanoparticles have shown a powerful antioxidant activity in many research studies. However, the possible neuroprotective effects of selenium nanoparticles in chronic stress remains to be elucidated.
In the present study, fifty rats were divided into three groups; control group (n=10), untreated CRS group (n=10) and CRS-SeNPs treated group (n=30). Restraint stress was performed by placing the rats in plastic bottles 6 hrs./day for 21 days. Rats of CRS-SeNPs treated group received 1, 2.5 or 5 mg/kg SeNPs (10 rats each) by oral gavage for 21 days. Body weight of rats was recorded on days 7, 14 and 21 of the study. At the end of the study, rats were subjected to behavioral assessments by elevated plus maze test, open filed test, forced swim test and sucrose preference test. Then, they were sacrificed for biochemical analysis of the prefrontal cortex and hippocampus. Prefrontal cortical and hippocampal serotonin, oxidative stress markers including MDA, reduced glutathione and glutathione peroxidase, TNF-and caspase-3 levels were assessed. Histological analysis of the prefrontal cortex and hippocampus was also performed.
The present work observed that chronic restraint stress induced anxiety-like and depressive-like behavior, decreased prefrontal cortical and hippocampal serotonin, caused marked oxidative stress, neuroinflammation and apoptosis compared to the control group. No effect on the body weight was shown. In addition, histological analysis illustrated disorganized prefrontal cortical and hippocampal architecture with evidence of neuronal loss. Treatment with different doses of selenium nanoparticles variably prevented such derangements, with the 2.5 mg/kg dose showing the best improving results in all studied parameters.
Based on the data above, the present study showed that selenium nanoparticles prevented the decrease in prefrontal cortical and hippocampal serotonin levels, improved behavioral parameters and preserved the normal histological architecture of the prefrontal cortex and hippocampus following exposure to chronic stress. In addition, the antioxidant, anti-inflammatory and anti-apoptotic effects of selenium nanoparticles are the possible mechanisms for these effects.