Low on energy? An energy supply-demand perspective on stress and depression. (November 2018)

• Record Type: Journal Article
• Authors: Østergaard, Leif; Jørgensen, Martin Balslev; Knudsen, Gitte Moos
• Is Part Of: Neuroscience and biobehavioral reviews. Volume 94(2018)
• Page Start: 248
• Page End: 270
• Publication Date: 2018-11
• Subjects: 5-HT 5-hydroxytryptamine -- AA arachidonic acid -- ACh acetylcholine -- ACTH adrenocorticotrophic hormone -- AD Alzheimer's Disease -- ADP adenosine diphosphate -- Aβ amyloid β -- AMP adenosine monophosphate -- AMPA α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid -- AMPK AMP-activated kinase -- AT2 angiotensin II -- ATP adenosine triphosphate -- AVP arginine vasopressin -- BBB blood-brain barrier -- BDNF brain derived neurotrophic factor -- BOLD blood oxygen level dependent -- CBF cerebral blood flow -- CBV cerebral blood volume -- CRH corticotrophin releasing hormone -- CRP C reactive protein -- CSF cerebrospinal fluid -- CTH capillary transit-time heterogeneity -- CUS chronic unpredictable stress -- DBS deep brain stimulation -- DG dentate gyrus -- EAAT excitatory amino acid transporters -- ECT electroconvulsive therapy -- EPC endothelial progenitor cell -- fMRI functional magnetic resonance imaging -- FST forced swimming test -- GC glucocorticoid -- GR glucocorticoid receptor -- HIF hypoxia inducible factor -- HPA hypothalamic-pituitary-adrenal -- ICAM-1 intercellular adhesion molecule 1 -- IL-1 interleukin-1 -- LC locus coeruleus -- LPS lipopolysaccharides -- LTP long term potentiation -- MRI magnetic resonance imaging -- mtDNA maternal DNA -- mTOR mammalian target of rapamycin -- MTT mean transit time -- MDD major depressive disorder -- NA noradrenaline -- NADPH nicotinamide adenine dinucleotide phosphate -- NF-κB nuclear factor kappa beta -- NMDA N-methyl-D-aspartate -- NO nitric oxide -- OEF oxygen extraction fraction -- PDE phosphodiesterase -- PET positron emission tomography -- PH prolyl hydroxylase -- PVN paraventricular nucleus of the hypothalamus -- RA rheumatoid arthritis -- RBC red blood cell -- ROS reactive oxygen species -- SMA sympathetic-medullo-adrenergic -- VSMC vascular smooth muscle cell -- SRI serotonin reuptake inhibitor -- SSRI selective serotonin uptake inhibitor -- SVD cerebral small vessel disease -- TNF-α tumor necrosis factor-α -- VCAM-1 vascular cell adhesion molecule 1 -- VEGF vascular endothelial growth factor -- WMH white matter hyperintensities; Stress -- Major depressive disorder(MDD) -- Early life stress -- Cardiovascular disease -- Inflammation -- Capillary dysfunction -- Cortisol -- Hippocampus -- Neurodegeneration -- Trophic support -- Hypoxia -- Gut -- Catecholamines -- Serotonin -- Glutamate -- Pericyte -- Glycocalyx -- Blood viscosity -- Hemorheology -- Neuroimaging -- Functional magnetic resonance imaging (fMRI) -- Co-morbidity -- Alzheimer's Disease (AD) -- Cerebral small vessel disease (SVD) -- White matter hyperintensities (WMHs) -- Pathophysiology; Psychophysiology -- Periodicals; Human behavior -- Periodicals; Animal behavior -- Periodicals; Neurology -- Periodicals; Behavior -- Periodicals; Ethology -- Periodicals; Neurology -- Periodicals; Psychophysiologie -- Périodiques; Comportement humain -- Périodiques; Animaux -- Mœurs et comportement -- Périodiques; Neurologie -- Périodiques; Animal behavior; Human behavior; Neurology; Psychophysiology; Periodicals; Electronic journals; 573.8
• DOI: 10.1016/j.neubiorev.2018.08.007
• Languages: English
• ISSNs: 0149-7634

Abstract

Graphical abstract: Highlights: Reduced ATP or oxygen availability is common in depression models, human depression, and depression risk factors. Capillary dysfunction can cause tissue hypoxia, even when blood supply is inconspicuous. Tissue hypoxia triggers inflammation, affecting capillary function in other organs. Inflammatory cytokines and tissue hypoxia interfere with neurotransmitter synthesis. Early life stress may predispose to depression and other diseases in later life by damaging the splanchnic microcirculation. Capillary function and neurogenic blood flow affect brain oxygenation, and whether functional neuroimaging truly detects changes in neuronal activity. Abstract: 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.