Stress reduction

“Stress reduction” does not refer to any single molecule or receptor, but instead describes an overall decrease in physiological and psychological responses associated with acute or chronic exposure to stressful stimuli. The biological processes underlying “stress” involve complex networks including: - Activation of the sympathetic nervous system (“fight-or-flight” response) via catecholamines like epinephrine/adrenaline, - Engagement of the hypothalamic-pituitary-adrenal axis leading to release of corticotropin-releasing hormone (CRH), adrenocorticotropic hormone (ACTH), and glucocorticoids such as cortisol, - Modulation by neurotransmitters including serotonin and gamma aminobutyric acid, - Involvement of intracellular signaling pathways affecting synaptic plasticity—such as those mediated by Src kinase—and changes at tight junctions within brain vasculature influencing blood-brain barrier permeability, - Regulation through nuclear receptors like mineralocorticoid receptors and glucocorticoid receptors which mediate genomic responses following corticosteroid binding[3][4][5]. Therapeutic strategies aimed at “stress reduction” may therefore act on many different targets depending on their mechanism—none are called “the Stress Reduction Receptor.” Thus “Stress Reduction” should not be treated as a canonical drug target name, but rather as an outcome achieved through modulation across several well-defined biological systems[1].

Other names

Stress reliefAnxiolysisReduction of stress response

Null for this entry directly. However: Drugs that reduce symptoms associated with stress act via diverse mechanisms including modulation of neurotransmitter systems (serotonin reuptake inhibition by SSRIs; enhancement of GABAergic transmission by benzodiazepines), inhibition of specific kinases involved in synaptic plasticity under chronic stress conditions (e.g., Src kinase inhibitors), and regulation of neuroendocrine axes such as the hypothalamic-pituitary-adrenal [HPA] axis.