Rubab Batool 

Emotional stress known as intangible aspect that can induce anxiety, depression and stress related disorders. It has long and established relationship with physiology of living organisms. During aversive stimuli, body automatically activates many biological processes that can challenge the homeostatic environment of individuals. Emotional stress is categorized as adaptive (short term or acute) or maladaptive (long term or chronic). Acute stress response is a natural defense mechanism against stress and known as “fight or flight” or “wear-and-tear”. Whereas chronic stress can result in disruption of various physiological processes (atrophy of the brain mass and decrease its weight, cognition and learning, mood, immune system, cancer and cardiovascular) leading to many physiological conditions 

Chronic stress contribute in psychological disorders via anxiety and depression by activating functions of amygdala while increasing structural degeneration in the hippocampus and prefrontal cortex (PFC). Chronic stress response take control over hippocampus and PFC by inhibiting them. Neuronal structures include different parts of brain such as amygdale which is associated with neuro-circuitry of fear and respond to emotional threat to maintain homeostasis. Much has been investigated about the role of stress hormones and their related responses but little is known about the source genes which contribute in the activation of stress response. In this study, we use C57BL/6 mice model to induce emotional stress to analyze its impact on the expression of neuronal structure genes. mRNA expression of stress bio-marker Bdnf, Fkbp5 and Slc6a4 associated with anxiety, depression and cognitive impairment were quantified. We also examined expression of Npy, Comt, Ppm1f and Adra2b to identify their role in chronic stress. Biochemical, Histopathology and behavioral studies were also performed to understand the physiological effect of chronic stress. We observed increased expression of  Adra2b and Bdnf while decreased expression of  Fkbp5, Slc6a4, Comt, Ppm1f and Adra2b in emotionally compromised mice. Biochemical and histopathology data showed deregulated blood profile and impaired brain cell structure. Taken together we have demonstrated that anxiety, depression and stress not only induce deformity in cellular structure of brain but also affect the pattern of expression of neuronal structure genes leading to disorders.