TY - JOUR

T1 - Low on energy?

T2 - An energy supply-demand perspective on stress and depression

AU - Østergaard, Leif

AU - Jørgensen, Martin Balslev

AU - Knudsen, Gitte Moos

N1 - Copyright © 2018 Elsevier Ltd. All rights reserved.

PY - 2018

Y1 - 2018

N2 - Are energy demands too high, or our energy resources either too low or inappropriately prioritized, as we develop stress and/or depression? We review evidence of dysregulated cellular energy homeostasis and energy depletion in stress and depression, identifying factors that might limit energy substrate availability. Resetting of cellular energy-sensors, splanchnic hypoxia, and catecholamine effects on blood viscosity emerge as mechanisms that might disrupt normal energy homeostasis, accelerate cell injury, and cause depression-like symptoms in severe or prolonged stress. In particular, a vicious cycle of capillary dysfunction, cellular hypoxia, and inflammation emerges as a mechanism, by which prolonged stress might accelerate the development of diseases, including depression, in later life. Oxygen is a substrate for both serotonin- and ATP-synthesis, and the review therefore analyzes evidence of reduced oxygen availability in neurological diseases with high incidence of depression. Blood supply and oxygen availability are also keys to the inference of neuronal activity by functional neuroimaging. We review how neurotransmitters interfere with blood flow regulation, affecting interpretations of neuroimaging studies in stress and depression.

AB - Are energy demands too high, or our energy resources either too low or inappropriately prioritized, as we develop stress and/or depression? We review evidence of dysregulated cellular energy homeostasis and energy depletion in stress and depression, identifying factors that might limit energy substrate availability. Resetting of cellular energy-sensors, splanchnic hypoxia, and catecholamine effects on blood viscosity emerge as mechanisms that might disrupt normal energy homeostasis, accelerate cell injury, and cause depression-like symptoms in severe or prolonged stress. In particular, a vicious cycle of capillary dysfunction, cellular hypoxia, and inflammation emerges as a mechanism, by which prolonged stress might accelerate the development of diseases, including depression, in later life. Oxygen is a substrate for both serotonin- and ATP-synthesis, and the review therefore analyzes evidence of reduced oxygen availability in neurological diseases with high incidence of depression. Blood supply and oxygen availability are also keys to the inference of neuronal activity by functional neuroimaging. We review how neurotransmitters interfere with blood flow regulation, affecting interpretations of neuroimaging studies in stress and depression.

KW - Animals

KW - Blood Circulation

KW - Depression/metabolism

KW - Depressive Disorder/metabolism

KW - Humans

KW - Models, Biological

KW - Oxygen/metabolism

KW - Stress, Psychological/metabolism

U2 - 10.1016/j.neubiorev.2018.08.007

DO - 10.1016/j.neubiorev.2018.08.007

M3 - Review

C2 - 30145282

VL - 94

SP - 248

EP - 270

JO - Neuroscience & Biobehavioral Reviews

JF - Neuroscience & Biobehavioral Reviews

SN - 0149-7634

ER -