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Part of the book series: Experientia Supplementum ((EXS,volume 95))

Conclusions

NPY is a mediator and a marker of chronic stress in humans, including extreme trauma and PTSD, but its actions are complex. In the periphery, as a sympathetic neurotransmitter, it exerts excitatory effects on the cardiovascular system and modulates immune responses. In contrast, in the central nervous system, NPY-ergic neurons are powerful inhibitory, anti-stress and anxiolytic system. In PTSD, stress-induced elevations of plasma NPY are associated with increases in cortisol, catecholamines and blood pressure, consistent with peptide’s actions in the cardiovascular system. However, lower plasma NPY levels, baseline, stress-induced, and/or post-stress are associated with poorer behavioral performance under stress — suggesting that reduced activity of the central NPY system diminishes individual’s stress resilience. Many of the peripheral pro-stress and central anti-stress actions of NPY appears to be mediated by the same subtype of receptors, the Y1, which complicates the case of using Y1 antagonists for treatment of stress-related cardiovascular and immune symptoms, unless drugs which do not penetrate the blood-brain-barrier are used. Future studies should determine more precise mechanisms of NPY’s actions and type of receptors involved in psychological, behavioral, cardiovascular and immune consequences of chronic stress, particularly PTSD, where peptide’s role appears to be quite compelling.

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Dutton, M.A., Lee, E.W., Zukowska, Z. (2006). NPY and extreme stress: lessons learned from posttraumatic stress disorder. In: Zukowska, Z., Feuerstein, G.Z. (eds) NPY Family of Peptides in Neurobiology, Cardiovascular and Metabolic Disorders: from Genes to Therapeutics. Experientia Supplementum, vol 95. Birkhäuser Basel. https://doi.org/10.1007/3-7643-7417-9_16

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