ArticlePloS one2011
Region-specific expression of mitochondrial complex I genes during murine brain development.
Article in PloS one, 2011. 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, 26 citations in OpenAlex.
- Nuclear hormone receptors control fundamental processes of human fetal neurodevelopment: Basis for endocrine disruption assessment.Environment international · 2025Article
- Raptor-Mediated Proteasomal Degradation of Deamidated 4E-BP2 Regulates Postnatal Neuronal Translation and NF-κB Activity.Cell reports · 2019Article
- FOXRED1 silencing in mice: a possible animal model for Leigh syndrome.Metabolic brain disease · 2019Article
- DNA repair deficiency in neuropathogenesis: when all roads lead to mitochondria.Translational neurodegeneration · 2019Review
- Differential Alterations of the Mitochondrial Morphology and Respiratory Chain Complexes during Postnatal Development of the Mouse Lung.Oxidative medicine and cellular longevity · 2017Article
- Imaging mass spectrometry reveals loss of polyunsaturated cardiolipins in the cortical contusion, hippocampus, and thalamus after traumatic brain injury.Journal of neurochemistry · 2016Article
- Mutations in Subunits of the Activating Signal Cointegrator 1 Complex Are Associated with Prenatal Spinal Muscular Atrophy and Congenital Bone Fractures.American journal of human genetics · 2016Article
- Energy and Potassium Ion Homeostasis during Gamma Oscillations.Frontiers in molecular neuroscience · 2016Review
- Highly energized inhibitory interneurons are a central element for information processing in cortical networks.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2014Review
- Imaging mass spectrometry of diversified cardiolipin molecular species in the brain.Analytical chemistry · 2014Article
- Molecular patterns of neurodevelopmental preconditioning: a study of the effects of antenatal steroid therapy in a protein-restriction mouse model.ISRN obstetrics and gynecology · 2014Article
- Creb1-Mecp2-(m)CpG complex transactivates postnatal murine neuronal glucose transporter isoform 3 expression.Endocrinology · 2013Article
- OXPHOS mutations and neurodegeneration.The EMBO journal · 2013Review
- The energy demand of fast neuronal network oscillations: insights from brain slice preparations.Frontiers in pharmacology · 2011Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mutations in the nuclear encoded subunits of mitochondrial complex I (NADH:ubiquinone oxidoreductase) may cause circumscribed cerebral lesions ranging from degeneration of the striatal and brainstem gray matter (Leigh syndrome) to leukodystrophy. We hypothesized that such pattern of regional pathology might be due to local differences in the dependence on complex I function. Using in situ hybridization we investigated the relative expression of 33 nuclear encoded complex I subunits in different brain regions of the mouse at E11.5, E17.5, P1, P11, P28 and adult (12 weeks). With respect to timing and relative intensity of complex I gene expression we found a highly variant pattern in different regions during development. High average expression levels were detected in periods of intense neurogenesis. In cerebellar Purkinje and in hippocampal CA1/CA3 pyramidal neurons we found a second even higher peak during the period of synaptogenesis and maturation. The extraordinary dependence of these structures on complex I gene expression during synaptogenesis is in accord with our recent findings that gamma oscillations--known to be associated with higher cognitive functions of the mammalian brain--strongly depend on the complex I activity. However, with the exception of the mesencephalon, we detected only average complex I expression levels in the striatum and basal ganglia, which does not explain the exquisite vulnerability of these structures in mitochondrial disorders.
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