ArticlePloS one2013
Mitochondrial functional state impacts spontaneous neocortical activity and resting state FMRI.
Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed.
- Functional Connectivity, Tissue Microstructure, and T2 at 11.1 Tesla Distinguishes Neuroadaptive Differences in Two Traumatic Brain Injury Models in Rats: A Translational Outcomes Project in NeuroTrauma (TOP-NT) UG3 Phase Study.Neurotrauma reports · 2025Article
- Spatiotemporal relationships between neuronal, metabolic, and hemodynamic signals in the awake and anesthetized mouse brain.Cell reports · 2024Article
- Sex-based structural and functional MRI outcomes in the rat brain after soman (GD) exposure-induced status epilepticus.Epilepsia open · 2023Article
- Ru360 Alleviates Postoperative Cognitive Dysfunction in Aged Mice by Inhibiting MCU-Mediated Mitochondrial Dysfunction.Neuropsychiatric disease and treatment · 2023Article
- Frontal-posterior functional imbalance and aberrant function developmental patterns in schizophrenia.Translational psychiatry · 2021Article
- Traumatic brain injury metabolome and mitochondrial impact after early stage Ru360 treatment.Mitochondrion · 2021Article
- How Energy Supports Our Brain to Yield Consciousness: Insights From Neuroimaging Based on the Neuroenergetics Hypothesis.Frontiers in systems neuroscience · 2021Review
- Kaempferol Treatment after Traumatic Brain Injury during Early Development Mitigates Brain Parenchymal Microstructure and Neural Functional Connectivity Deterioration at Adolescence.Journal of neurotrauma · 2020Article
- Beneficial Effects of Kaempferol after Developmental Traumatic Brain Injury Is through Protection of Mitochondrial Function, Oxidative Metabolism, and Neural Viability.Journal of neurotrauma · 2019Article
- Alterations of Parenchymal Microstructure, Neuronal Connectivity, and Cerebrovascular Resistance at Adolescence after Mild-to-Moderate Traumatic Brain Injury in Early Development.Journal of neurotrauma · 2019Article
- Infraslow Electroencephalographic and Dynamic Resting State Network Activity.Brain connectivity · 2017Article
- Biomarkers, designs, and interpretations of resting-state fMRI in translational pharmacological research: A review of state-of-the-Art, challenges, and opportunities for studying brain chemistry.Human brain mapping · 2017Review
- Mitochondrial calcium homeostasis: Implications for neurovascular and neurometabolic coupling.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2017Review
- A Mitochondrial Biomarker-Based Study of S-Equol in Alzheimer's Disease Subjects: Results of a Single-Arm, Pilot Trial.Journal of Alzheimer's disease : JAD · 2017Article
- Energetic Constraints Produce Self-sustained Oscillatory Dynamics in Neuronal Networks.Frontiers in neuroscience · 2017Article
- Facilitating Mitochondrial Calcium Uptake Improves Activation-Induced Cerebral Blood Flow and Behavior after mTBI.Frontiers in systems neuroscience · 2016Article
- Protective Effects of Quercetin on Mitochondrial Biogenesis in Experimental Traumatic Brain Injury via the Nrf2 Signaling Pathway.PloS one · 2016Article
- Preclinical Magnetic Resonance Imaging and Spectroscopy Studies of Memory, Aging, and Cognitive Decline.Frontiers in aging neuroscience · 2016Review
- Role of mitochondrial calcium uptake homeostasis in resting state fMRI brain networks.NMR in biomedicine · 2015Article
Corrections and comments
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Authors and funding
4 authors.
Funding
Abstract
Mitochondrial Ca(2+) uptake, central to neural metabolism and function, is diminished in aging whereas enhanced after acute/sub-acute traumatic brain injury. To develop relevant translational models for these neuropathologies, we determined the impact of perturbed mitochondrial Ca(2+) uptake capacities on intrinsic brain activity using clinically relevant markers. From a multi-compartment estimate of probable baseline Ca(2+) ranges in the brain, we hypothesized that reduced or enhanced mitochondrial Ca(2+) uptake capacity would decrease or increase spontaneous neuronal activity respectively. As resting state fMRI-BOLD fluctuations and stimulus-evoked BOLD responses have similar physiological origins [1] and stimulus-evoked neuronal and hemodynamic responses are modulated by mitochondrial Ca(2+) uptake capacity [2], [3] respectively, we tested our hypothesis by measuring hemodynamic fluctuations and spontaneous neuronal activities during normal and altered mitochondrial functional states. Mitochondrial Ca(2+) uptake capacity was perturbed by pharmacologically inhibiting or enhancing the mitochondrial Ca(2+) uniporter (mCU) activity. Neuronal electrical activity and cerebral blood flow (CBF) fluctuations were measured simultaneously and integrated with fMRI-BOLD fluctuations at 11.7T. mCU inhibition reduced spontaneous neuronal activity and the resting state functional connectivity (RSFC), whereas mCU enhancement increased spontaneous neuronal activity but reduced RSFC. We conclude that increased or decreased mitochondrial Ca(2+) uptake capacities lead to diminished resting state modes of brain functional connectivity.
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