ABSTRACT
Background and Aim: Depression and anxiety are the most prominent neuropsychiatric disease and have been considered as the most burdensome diseases of society. The hippocampus and prefrontal cortex have a prominent role in stress-induced neurological disorders. Chronic unpredictable stress exposed rats are a perfect model in understanding comorbid depression and anxiety disorders. The inflammatory response occurring in the body has been linked to C-reactive protein (CRP) in many diseased conditions. The present research primarily focus on the possible correlation of Cortisol, CRP level and neuronal assay in different regions of hippocampus, dentate gyrus (DG), and prefrontal cortex.
Materials and Methods: The control group of rats (n=6) was not exposed to any stress. Whereas, the experimental stress group (n=6) of rats was exposed to various stressors for 15 days. After the experimentation procedures, the blood samples were collected and brain dissection was done. The neurons in the prefrontal cortex, the DG along with various hippocampal regions was counted. Statistical analysis was performed using student's t-test and p<0.05 was expressed as statistically significant.
Results: Animals exposed to chronic unpredictable stressors showed a significant (p<0.0001) decrease in the neuronal count in prefrontal cortex and hippocampus. A significant rise in the serum cortisol (p<0.0001) and CRP (p<0.001) was witnessed in the stressed group.
Conclusion: Our results demonstrate that chronic unpredictable stress exposure has affected neurogenesis in prefrontal cortex and hippocampal regions. Decreased neurogenesis was well in coordinance with the increase in cortisol and CRP. The chronic unpredictable stress-induced inflammatory response correlated to various brain regions might provoke insights into a variety of new drugs targeting neurogenesis.
Keywords: anxiety, C reactive protein, cortisol, depression, neuronal count, rat model, stress.
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