Neuroscience and Psychiatry: Open Access

Adaptation Impact Factor:

  Stress initiates adaptive mechanisms that physiologically allow the organism to cope with sustained or sporadic exposure to actual or perceived risks. Repeated induction of glucocorticoid secretion by the hypothalamo-pituitary-adrenocortical (HPA) axis, which stimulates energy transfer in a broad variety of organs including the brain, is a major component of the answer. Prolonged or chronic changes in glucocorticoid secretion may limit the advantages of improved reactivity to stress and ultimately become ill-adaptive. The long-term effect of stress is regulated by the habituations cycle, which reduces the reaction of the HPA axis after sustained exposure. Limits deleterious behavior of excessive glucocorticoid production of homotypical stressors and possibly. Habituations are influenced by limbic stress-regulating locations, which are at least partially based on glucocorticoid input. Chronic stress also makes reactivity more sensitive to new stimuli. Although sensitization can be critical in preserving resilience in reaction to new challenges, it can also contribute to the combined brain and body effect of glucocorticoids. Finally, unpredictable or severe exposure to stress can cause long-term and lasting dysregulation of the HPA axis, most likely due to altered limbic control of the pathways of the stress effector. Disorders relating to stress, such as depression and PTSD.The organismic reaction to stress (defined here as a real or perceived threat to homeostasis or well-being) facilitates survival through changes to ongoing physiological processes and behaviour. The activation of multiple processes of interaction, including the behavioral, autonomic, endocrine and immune systems, produces an integrated response to stress.  

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