The serious mental disorder known as major depressive disorder has a significant impact on a person's quality of life. Although the causes of this condition are still unknown, there has been growing attention on the impact that psychological stress has on depression. Despite the lack of adequate animal models of psychological stress, important strides have been made toward understanding the physiopathology underlying depression and treating its symptoms. Therefore, in order to improve our understanding of this condition, we will study both traditional models and novel methodologies.

Sensory nerve systems translate signals from external stresses like imminent risk to life, social stressors, and reactions to physical injuries before the subsequent information is processed by the brain's so-called emotional circuits [16]. Although the neuronal circuits underlying the pathology of depression are still largely unknown to us, the variety of depression symptoms suggests that many different brain regions may be implicated in the affective problems. Amygdala, striatum, hippocampus, prefrontal and cingulate cortex, among other brain regions, have shown altered hemorheology and related parameters in human brain imaging investigations. Studies on the autopsied brains of depressive individuals have also revealed several abnormalities in those regions.

Decreased grey-matter volumes and decreased glial densities of the hippocampus and prefrontal cortex (PFC) in depressive patients are the most frequently reported findings obtained by brain-imaging technology, though it is still unclear whether these alterations in the hippocampus and PFC represent a precipitating factor or are simply a result of major depression.

Prefrontal Cortex

Despite the lack of a clear pro-depressant mechanism, social defeat-induced depression mouse models exhibit decreased medial PFC (mPFC) neuronal activity [21b]. Glial loss in the PFC and the degeneration of astrocytes in the PFC of rats both efficiently produced depressed symptoms and behaviours. In the PFC of depressed patients who committed suicide, the ERK1/2 MAPK pathway activity as well as the levels of mRNA expression and protein of ERK1/2 drastically decreased. P2X2 receptors in PFC were found to influence the antidepressant effects of ATP.

Recent research demonstrated that the prelimbic region of the medial prefrontal cortex (mPFC), in particular, regulates the vulnerability to stressful events. Cholecystokinin (CCK)-Breceptor activity is suppressed by the overexpression of the transcription factor FosB, which increases the vulnerability to stress [21b]. A pliable phenotype is produced in mice by blocking the CCKB receptor, while depressive symptoms resembling those brought on by social defeat stress are produced in mice by administering the ligand CCK to the mPFC [21b]..

International Journal of Emergency Mental Health and Human Resilience, is a multidisciplinary quarterly designed to be the premier international forum and authority for the discussion of all aspects of emergency mental health.

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International Journal of Emergency Mental Health and Human Resilience