Memory functions can be considerably affected by various life events and stress has shown to be a chief regulator. Different stress patterns have distinct effects on the overall functioning of the brain. Stress provokes inflammation not only in the periphery but also in the brain. Neuroinflammation causes alterations in neuronal structure and function, which eventually progress to the development of neurodegenerative diseases. Inflammatory reactions are modulated through communication between the nervous, endocrine and immune systems. An excessive release of stress hormones and changes in the neurotransmission system may cause cognitive impairments. The present study investigated dissimilar stress-related memory deficits and their diminution by non-steroidal anti-inflammatory drugs (NSAIDs). Treatment with cyclooxygenase inhibitors, which inhibit prostaglandin synthesis, has enhanced memory functions in a number of neuroinflammatory states. In this study, rats were exposed to a series of dissimilar stressors and behavioral parameters for depression and memory functions were examined. Corticosterone, serotonin (5-HT) and dopamine (DA) levels were also estimated. Results from the forced swim test, elevated plus maze test and Morris water maze test showed significant effects of NSAIDs. A significant decrease in plasma corticosterone and increased DA and 5-HT levels were observed in NSAID-treated dissimilar-stressed rats. This study demonstrates the therapeutic potential of NSAIDs for dissimilar stress-induced depressive behaviors and impaired memory functions and related hormonal and neurochemical changes in the rat brain.

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http://dx.doi.org/10.1016/j.neuroscience.2017.11.014DOI Listing

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