ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2006
Abnormal Ca2+ dynamics in transgenic mice with neuron-specific mitochondrial DNA defects.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 40 citations in OpenAlex.
- Functional and behavioral effects of de novo mutations in calcium-related genes in patients with bipolar disorder.Human molecular genetics · 2021Article
- The Role of Mitonuclear Incompatibility in Bipolar Disorder Susceptibility and Resilience Against Environmental Stressors.Frontiers in genetics · 2021Review
- Unbiased PCR-free spatio-temporal mapping of the mtDNA mutation spectrum reveals brain region-specific responses to replication instability.BMC biology · 2020Article
- Reply to "Correspondence to Ant1 mutant mice bridge the mitochondrial and serotonergic dysfunctions in bipolar disorder".Molecular psychiatry · 2020Article
- Molecular Mechanisms Linking ALS/FTD and Psychiatric Disorders, the Potential Effects of Lithium.Frontiers in cellular neuroscience · 2019Review
- Ant1 mutant mice bridge the mitochondrial and serotonergic dysfunctions in bipolar disorder.Molecular psychiatry · 2018Article
- Are Polyunsaturated Fatty Acids Implicated in Histaminergic Dysregulation in Bipolar Disorder?: AN HYPOTHESIS.Frontiers in physiology · 2018Review
- Expanding the toolbox of ADHD genetics. How can we make sense of parent of origin effects in ADHD and related behavioral phenotypes?Behavioral and brain functions : BBF · 2015Review
- Mitochondrial dysfunction in psychiatric morbidity: current evidence and therapeutic prospects.Neuropsychiatric disease and treatment · 2015Review
- Frontal lobe bioenergetic metabolism in depressed adolescents with bipolar disorder: a phosphorus-31 magnetic resonance spectroscopy study.Bipolar disorders · 2012Article
- Impaired mitochondrial function in psychiatric disorders.Nature reviews. Neuroscience · 2012Review
- Evidence for selective microRNAs and their effectors as common long-term targets for the actions of mood stabilizers.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2009Article
- Mouse models of oxidative phosphorylation dysfunction and disease.Methods (San Diego, Calif.) · 2008Article
- A marked effect of electroconvulsive stimulation on behavioral aberration of mice with neuron-specific mitochondrial DNA defects.PloS one · 2008Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Maintenance of mitochondrial DNA (mtDNA) depends on nuclear-encoded proteins such as mtDNA polymerase (POLG), whose mutations are involved in the diseases caused by mtDNA defects including mutation and deletion. The defects in mtDNA and in intracellular Ca2+ ([Ca2+]i) homeostasis have been reported in bipolar disorder (BD). To understand the relevance of the mtDNA defects to BD, we studied transgenic (Tg) mice in which mutant POLG (mutPOLG) was expressed specifically in neurons. mtDNA defects were accumulated in the brains of mutPOLG Tg mice in an age-dependent manner and the mutant mice showed BD-like behavior. However, the molecular and cellular basis for the abnormalities has not been clarified. In this study, we investigated Ca2+ regulation by isolated mitochondria and [Ca2+]i dynamics in the neurons of mutPOLG Tg mice. Mitochondria from the mutant mice sequestered Ca2+ more rapidly, whereas Ca2+ retention capacity and membrane potential, a driving force of Ca2+ uptake, of mitochondria were unaffected. To elucidate the molecular mechanism of the altered Ca2+ uptake, we performed DNA microarray analysis and found that the expression of cyclophilin D (CyP-D), a component of the permeability transition pore, was downregulated in the brains of mutPOLG Tg mice. Cyclosporin A, an inhibitor of CyP-D, mimicked the enhanced Ca2+ uptake in mutant mice. Furthermore, G-protein-coupled receptor-mediated [Ca2+]i increase was attenuated in hippocampal neurons of the mutant mice. These findings suggest that mtDNA defects lead to enhancement of Ca2+ uptake rate via CyP-D downregulation and alter [Ca2+]i dynamics, which may be involved in the pathogenesis of BD.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.