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Mood Mitochondria and



  • Mood Mitochondria and
  • Mitochondrial Functions in Mood Disorders
  • chapter and author info
  • Front Neurosci. Jun 6; doi: /fnins eCollection Mitochondria and Mood: Mitochondrial Dysfunction as a Key Player in the. Human and animal studies suggest an intriguing link between mitochondrial diseases and depression. Although depression has historically. Most of us have heard about the mitochondria in high school biology class. It's a part of all our cells (except red blood cells) and is considered.

    Mood Mitochondria and

    While attributing mood to a chemical has been long accepted, it may be a while before people accept the idea that changing mitochondrial movement statistics might better captures the effect.

    Mitochondria source more than just ATP and calcium to various parts of the cell. As new probes like voltage and calcium imaging, and established techniques like Patch clamping are applied to mitochondria, a finer-grained picture of their correlations to the larger spiking activity of neurons may emerge.

    The critical tool for observing mitochondria may ultimately be high resolution temperature imaging. Might mitochondria move along temperature gradients inside a neuron. If so, in what direction? Please sign in to add a comment. Registration is free, and takes less than a minute.

    Your feedback will go directly to Science X editors. Thank you for taking your time to send in your valued opinion to Science X editors. You can be assured our editors closely monitor every feedback sent and will take appropriate actions. Your opinions are important to us. We do not guarantee individual replies due to extremely high volume of correspondence.

    E-mail the story Controlling mood through the motions of mitochondria Your friend's email Your email I would like to subscribe to Science X Newsletter. Learn more Your name Note Your email address is used only to let the recipient know who sent the email. Neither your address nor the recipient's address will be used for any other purpose. The information you enter will appear in your e-mail message and is not retained by Medical Xpress in any form.

    You can unsubscribe at any time and we'll never share your details to third parties. More information Privacy policy. This site uses cookies to assist with navigation, analyse your use of our services, and provide content from third parties. By using our site, you acknowledge that you have read and understand our Privacy Policy and Terms of Use. Share Twit Share Email. Image by Ticipico, via Ed Yong. Controlling mood through the motions of mitochondria , May 23 retrieved 12 February from https: This document is subject to copyright.

    Apart from any fair dealing for the purpose of private study or research, no part may be reproduced without the written permission.

    The content is provided for information purposes only. Tracking HIV's ever-evolving genome in effort to prioritize public health resources 8 hours ago.

    Mitochondrial dynamics in neurons: Whats all the fuss about? Mutations in VCP gene implicated in a number of neurodegenerative diseases Mar 14, Researchers identify brain protein crucial to recovery from stroke 9 hours ago.

    Spinal cord is 'smarter' than previously thought 16 hours ago. What do you think about this particular story? Your message to the editors. Your email only if you want to be contacted back. E-mail the story Controlling mood through the motions of mitochondria. I would like to subscribe to Science X Newsletter. Note Your email address is used only to let the recipient know who sent the email. It would be of interest to map the dose-dependent effects of glucocorticoids on markers of mitochondrial function along with depression-like behavior to further confirm these relationships.

    There has been quite a bit of work done to try to understand the effect of antidepressant drugs on mitochondrial function. Much of the research done to examine links between antidepressant drugs and mitochondrial function have used the SSRI fluoxetine, which may either inhibit or trigger mitochondrial apoptosis and alter activity of the ETC, depending on the cell type de Oliveira, The same effects were found in a later study on the rat brain, with fluoxetine decreasing the rate of ATP synthesis Curti et al.

    These results indicate that high doses of fluoxetine have negative effects on mitochondria. Fluoxetine crosses mitochondrial membranes with ease, and it is possible that fluoxetine could interfere with membrane-bound proteins causing pro-apoptotic events de Oliveira, In vivo studies reveal a slightly more complex scenario, in that fluoxetine has both beneficial and detrimental effects on mitochondria when given systemically. Fluoxetine at the same dose also increased activity of ETC complex I in the hippocampus after one injection, but not in the prefrontal cortex or striatum Agostinho et al.

    However, after 28 days of daily injections, complex IV activity was decreased in the hippocampus. These results suggest sex and region specific effects of systemic fluoxetine on mitochondrial function.

    There has been some work done to examine the effect of other antidepressants. For example, chronic treatment with the tricyclic antidepressant imipramine as well as electroconvulsive shocks increased levels of cytochrome b mRNA in the rat cortex but not in the hippocampus, cerebellum or liver Huang et al. Finally, fluoxetine and desipramine enhanced cytochrome oxidase and glutamate dehydrogenase in presynaptic mitochondria located in the rat hippocampus Villa et al.

    These data highlight the importance of antidepressants at a subcellular level and suggest that mitochondrial energy metabolism could be a mechanism of antidepressant drug action. Women are more than twice as likely to suffer from depression than men, but it is not yet clear why this occurs and whether or not it has a biological basis. There is evidence that gender differences might arise due to decreased levels of circulating estrogens Bloch et al.

    Furthermore, administering estradiol alleviates depression-like symptoms in ovariectomized rats Rachman et al. The evidence linking mitochondria to estradiol and depression is sparse, but emerging. Some studies have indicated a protective role of estradiol in mitochondria, showing that it can inhibit the passage of ROS into mitochondria as well as preventing mitochondrial collapse and increasing the rate of ATP synthesis Wang et al.

    Mitochondria are known to express estrogen and GRs in lung tissue, suggesting that mitochondria are responsive to fluctuating levels of stress hormones and estradiol Walf and Frye, It would be quite interesting to follow these studies with an investigation of brain mitochondria and estrogen receptors to determine whether sex steroid hormones in the brain might be involved in the gender differences seen in the prevalence of depression.

    The specific biological mechanisms underlying major depression have yet to be elucidated. This review highlights the potential importance of mitochondrial function in depression. This is an area that has received relatively little experimental attention, but the data that have been published to date are promising and should be pursued.

    Although one must be cautious in extrapolating findings from preclinical animal models to the human condition, there is evidence that chronic stress-induced inhibition of ETC complexes in the inner membrane of mitochondria is a contributing factor in the pathophysiology of depression. Dysfunctional mitochondria decrease the pool of available ATP, which could have detrimental effects on signal transduction pathways, dampening activity in neuronal circuits, and interfering with mitochondrial fusion and fission.

    This negative cascade would ultimately increase oxidative stress, inflammatory responses, and pro-apoptotic events, some of which are known to be involved in the pathogenesis of depression. Viewed this way, it seems logical that reversing the early stages of mitochondrial dysfunction could provide a novel target for therapeutic intervention.

    All authors contributed to the writing of this manuscript. JA wrote the first draft. JA constructed the figure. LK finalized the manuscript. The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest. National Center for Biotechnology Information , U. Journal List Front Neurosci v. Published online Jun 6. Brymer , 2 Hector J. Caruncho , 1 and Lisa E.

    Author information Article notes Copyright and License information Disclaimer. This article was submitted to Neurodegeneration, a section of the journal Frontiers in Neuroscience. Received Feb 27; Accepted May The use, distribution or reproduction in other forums is permitted, provided the original author s and the copyright owner are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

    This article has been cited by other articles in PMC. Abstract Human and animal studies suggest an intriguing link between mitochondrial diseases and depression. Mitochondria Mitochondria are the main energy factories of eukaryotic cells. Open in a separate window. Genetics There have been many observations of links between mtDNA and depression.

    Oxidative Stress Mitochondria are the primary source of ROS, which under normal conditions play important roles in cell signaling and homeostasis. Reelin, Oxidative Stress, Inflammation, and Depression A further link between ROS and depression has been suggested by recent work focused on the extracellular matrix protein reelin. Apoptosis Mitochondria have a clear role in cell metabolism, and evidence suggests that mitochondrial morphology also affects metabolic enzymes through fusion and fission Chen et al.

    The Effect of Antidepressants on Mitochondria There has been quite a bit of work done to try to understand the effect of antidepressant drugs on mitochondrial function. Gender Differences in Depression and Mitochondria Women are more than twice as likely to suffer from depression than men, but it is not yet clear why this occurs and whether or not it has a biological basis. Conclusion The specific biological mechanisms underlying major depression have yet to be elucidated. Author Contributions All authors contributed to the writing of this manuscript.

    Conflict of Interest Statement The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest. Antidepressant action on mitochondrial dysfunction in psychiatric disorders. Brain region- and sex-specific modulation of mitochondrial glucocorticoid receptor phosphorylation in fluoxetine treated stressed rats: Olanzapine plus fluoxetine treatment alters mitochondrial respiratory chain activity in the rat brain.

    Olfactory bulbectomy in mice triggers transient and long-lasting behavioral impairments and biochemical hippocampal disturbances. Linking the biological underpinnings of depression: Mitochondrial dysfunction in depression.

    Reduction of prefrontal cortex glucose metabolism common to three types of depression. Proteomic analysis of the anterior cingulate cortex in the major psychiatric disorders: The expression of proapoptosis genes is increased in bipolar disorder, but not in schizophrenia. Neuroanatomical pattern of mitochondrial complex I pathology varies between schizophrenia, bipolar disorder and major depression.

    The mood-improving actions of antidepressants do not depend on neurogenesis but are associated with neuronal remodeling. Psychiatry 14 —, PKC regulates a farnesyl-electrostatic switch on K-Ras that promotes its association with Bcl-XL on mitochondria and induces apoptosis.

    Endocrine factors in the etiology of postpartum depression. Central nervous system trauma and stroke. Biochemical considerations for oxygen radical formation and lipid peroxidation. Chronic high corticosterone reduces neurogenesis in the dentate gyrus of adult male and female rats. Peripheral etanercept administration normalizes behavior, hippocampal neurogenesis, and hippocampal reelin and GABAA receptor expression in a preclinical model of depression.

    Mitochondrial involvement in brain function and dysfunction: Influence of mitochondrial enzyme deficiency on adult neurogenesis in mouse models of neurodegenerative diseases.

    Lower hippocampal volume in patients suffering from depression: The contribution of proteomic studies in humans, animal models, and after antidepressant treatments to investigate the molecular neurobiology of major depression.

    Reelin-related disturbances in depression: Abnormalities in mitochondrial structure in cells from patients with bipolar disorder. Mitochondrial fusion and fission in mammals.

    Mitochondria DNA change and oxidative damage in clinically stable patients with major depressive disorder. Disruption of fusion results in mitochondrial heterogeneity and dysfunction. Protective effects of resveratrol on mitochondrial function in the hippocampus improves inflammation-induced depressive-like behavior.

    The spectrum of hearing loss due to mitochondrial DNA defects. Mitochondrial outer membrane permeabilization during apoptosis: Brain bioenergetics and redox state measured by 31P magnetic resonance spectroscopy in unaffected siblings of patients with psychotic disorders.

    Reversible inhibition of cytochrome c oxidase, the terminal enzyme of the mitochondrial respiratory chain, by nitric oxide. Implications for neurodegenerative diseases. Total antioxidant capacity and total oxidant status in patients with major depression: Fluoxetine interacts with the lipid bilayer of the inner membrane in isolated rat brain mitochondria, inhibiting electron transport and F1F0-ATPase activity.

    Elevated level of DNA damage and impaired repair of oxidative DNA damage in patients with recurrent depressive disorder. The interplay between inflammation, oxidative stress, DNA damage, DNA repair and mitochondrial dysfunction in depression.

    Threshold effects and control of oxidative phosphorylation in nonsynaptic rat brain mitochondria. Molecular Biology of the Cell.

    Acute mental stress induces mitochondrial bioenergetic crisis and hyper-fission along with aberrant mitophagy in the gut mucosa in rodent model of stress-related mucosal disease.

    Fluoxetine and the mitochondria: Mitochondria at the neuronal presynapse in health and disease. Neuroimaging abnormalities in the subgenual prefrontal cortex: Psychiatry 3 —, — Subgenual prefrontal cortex abnormalities in mood disorders. Dynamic regulation of mitochondrial function by glucocorticoids. Protective effects of lamotrigine, aripiprazole and escitalopram on depression-induced oxidative stress in rat brain.

    Venlafaxine modulates depression-induced oxidative stress in brain and medulla of rat. Psychiatric comorbidity in 36 adults with mitochondrial cytopathies. Imipramine protects against the deleterious effects of chronic corticosterone on depression-like behavior, hippocampal reelin expression, and neuronal maturation.

    Proteomics and metabolomics analysis of a trait anxiety mouse model reveals divergent mitochondrial pathways. Chronic fluoxetine treatment directs energy metabolism towards the citric acid cycle and oxidative phosphorylation in rat hippocampal nonsynaptic mitochondria.

    Abnormal cellular energy and phospholipid metabolism in the left dorsolateral prefrontal cortex of medication-free individuals with bipolar disorder: Reduced hippocampal volume correlates with executive dysfunctioning in major depression. NMDA receptor activation induces mitochondrial dysfunction, oxidative stress and apoptosis in cultured neonatal rat cardiomyocytes.

    Alterations of mitochondrial function and correlations with personality traits in selected major depressive disorder patients. Plasma cortisol in depressive illness.

    Evaluation of the effectiveness of chronic antidepressant drug treatments in the hippocampal mitochondria — A proteomic study in an animal model of depression. Peroxiredoxin distribution in the mouse brain with emphasis on neuronal populations affected in neurodegenerative disorders. Chronic mild stress damages mitochondrial ultrastructure and function in mouse brain. The central executioners of apoptosis: Effect of repeated corticosterone injections and restraint stress on anxiety and depression-like behavior in male rats.

    Reduced activation in lateral prefrontal cortex and anterior cingulate during attention and cognitive control functions in medication-naive adolescents with depression compared to controls. Monoamine neurocircuitry in depression and strategies for new treatments. Protein transport into mitochondria. When to hospitalize patients at risk for suicide. Stress, hypercortisolism and corticosteroid receptors in depression: Antidepressant-like effect of quercetin in bulbectomized mice and involvement of the antioxidant defenses, and the glutamatergic and oxidonitrergic pathways.

    In vitro inhibition of mitochondrial respiratory rate by antidepressants. Chronic antidepressant treatments increase cytochrome b mRNA levels in mouse cerebral cortex. Mitochondrial DNA mutations and cognition: Altered expression of mitochondria-related genes in postmortem brains of patients with bipolar disorder or schizophrenia, as revealed by large-scale DNA microarray analysis. Depression and the birth and death of brain cells: Effect of different doses of corticosterone on depression-like behavior and HPA axis responses to a novel stressor.

    Disease-specific alterations in frontal cortex brain proteins in schizophrenia, bipolar disorder, and major depressive disorder. The Stanley Neuropathology Consortium. Crosstalk between metabolic and neuropsychiatric disorders. Neurobiological basis of depression: Mitochondrial respiration in peripheral blood mononuclear cells correlates with depressive subsymptoms and severity of major depression.

    Mice with neuron-specific accumulation of mitochondrial DNA mutations show mood disorder-like phenotypes. Psychiatry 11 —, Mitochondrial dysfunction in bipolar disorder. Mitochondrial DNA polymorphisms in bipolar disorder. Increased levels of a mitochondrial DNA deletion in the brain of patients with bipolar disorder.

    Changes in regional brain glucose metabolism measured with positron emission tomography after paroxetine treatment of major depression. Results from the National Comorbidity Survey. Blood flow and metabolism of the human brain in health and disease.

    A mitochondrial bioenergetic basis of depression. Major depression in adolescent children consecutively diagnosed with mitochondrial disorder.

    Molecular evidence for mitochondrial dysfunction in bipolar disorder. Mitochondrial membrane permeabilization in cell death. Role of nitric oxide in stress-induced anxiety: Long-term ovariectomy enhances anxiety and depressive-like behaviors in mice submitted to chronic unpredictable stress.

    Gene-environment interaction and the genetics of depression. The importance of dendritic mitochondria in the morphogenesis and plasticity of spines and synapses. ABCB1 gene polymorphisms are associated with the severity of major depressive disorder and its response to escitalopram treatment. Nitric oxide and peroxynitrite exert distinct effects on mitochondrial respiration which are differentially blocked by glutathione or glucose. Repeated exposure to corticosterone, but not restraint, decreases the number of reelin-positive cells in the adult rat hippocampus.

    The progressive development of depression-like behavior in corticosterone-treated rats is paralleled by slowed granule cell maturation and decreased reelin expression in the adult dentate gyrus.

    Reelin as a putative vulnerability factor for depression: Course of illness, hippocampal function, and hippocampal volume in major depression. Glutathione depletion, lipid peroxidation and mitochondrial dysfunction are induced by chronic stress in rat brain. Identification of proteomic signatures associated with depression and psychotic depression in post-mortem brains from major depression patients.

    The role of energy metabolism dysfunction and oxidative stress in schizophrenia revealed by proteomics. Reciprocal limbic-cortical function and negative mood: Depressive behaviour in children diagnosed with a mitochondrial disorder.

    Affective disorders, antidepressant drugs and brain metabolism. Homocysteine levels in schizophrenia and affective disorders-focus on cognition. Sequence and functional analyses of mtDNA in a maternally inherited family with bipolar disorder and depression. Mitochondrial thiols in antioxidant protection and redox signaling: The neurobiology of depression.

    Neuroendocrine aspects of hypercortisolism in major depression. Abnormalities of cAMP signaling in affective disorders: Genes linking mitochondrial function, cognitive impairment and depression are associated with endophenotypes serving precision medicine. Second messenger-regulated protein kinases in the brain: Reelin regulates postnatal neurogenesis and enhances spine hypertrophy and long-term potentiation.

    Possible role of mitochondrial permeability transition pore in the pathogenesis of Huntington disease. Estrogen alters behavior and forebrain c-fos expression in ovariectomized rats subjected to the forced swim test. Estrogen and response to sertraline in postmenopausal women with major depressive disorder: Mitochondrial dysfunction and psychiatric disorders.

    Inhibition of mitochondrial respiratory chain in brain of rats subjected to an experimental model of depression. Serotonin transporter clustering in blood lymphocytes as a putative biomarker of therapeutic efficacy in major depressive disorder. Serotonin 2A receptor clustering in peripheral lymphocytes is altered in major depression and may be a biomarker of therapeutic efficacy.

    Serotonin transporter clustering in blood lymphocytes of reeler mice. The coexpression of reelin and neuronal nitric oxide synthase in a subpopulation of dentate gyrus neurons is downregulated in heterozygous reeler mice. Differential effects of corticosterone on the colocalization of reelin and neuronal nitric oxide synthase in the adult hippocampus in wild type and heterozygous reeler mice.

    Oxidative stress induces mitochondrial dysfunction in a subset of autism lymphoblastoid cell lines in a well-matched case control cohort. Psychiatric disorders biochemical pathways unraveled by human brain proteomics. Tumor necrosis factor alpha inhibits oxidative phosphorylation through tyrosine phosphorylation at subunit I of cytochrome c oxidase.

    Mitochondrial Functions in Mood Disorders

    The MHI outperformed individual mitochondrial function measures. Elevated positive mood at night was associated with higher MHI, and nightly. More than half of mitochondrial disease patients have comorbid mood disorders, and mice with neuron-specific accumulation of mtDNA. Mitochondria and Mood: Mitochondrial Dysfunction as a Key Player in the Manifestation of Depression. Frontiers in Neuroscience, ;.

    chapter and author info



    The MHI outperformed individual mitochondrial function measures. Elevated positive mood at night was associated with higher MHI, and nightly.


    More than half of mitochondrial disease patients have comorbid mood disorders, and mice with neuron-specific accumulation of mtDNA.


    Mitochondria and Mood: Mitochondrial Dysfunction as a Key Player in the Manifestation of Depression. Frontiers in Neuroscience, ;.


    Mitochondrial dysfunctions are assuming an increasingly important role in hypotheses of mood disorders, bipolar disorder mainly. Recently discussed biological.


    The role of mitochondria in neurons is far more active than one might imagine. depression, and other mood and anxiety disorders have also been associated.


    Human and animal studies suggest an intriguing link between mitochondrial diseases and depression. Although depression has historically been linked to.


    A neurologist explains how to support you mitochondria for more energy and better mental health.

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