ArticleThe Journal of physiology2004
Impact of mitochondrial inhibition on excitability and cytosolic Ca2+ levels in brainstem motoneurones from mouse.
Article in The Journal of physiology, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
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Who cites it
31 citing papers in PubMed, 68 citations in OpenAlex.
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- A narrative review of the mechanisms and consequences of intermittent hypoxia and the role of advanced analytic techniques in pediatric autonomic disorders.Clinical autonomic research : official journal of the Clinical Autonomic Research Society · 2023Review
- Elevated ROS levels during the early development of Angelman syndrome alter the apoptotic capacity of the developing neural precursor cells.Molecular psychiatry · 2023Article
- Neurodegeneration in Multiple Sclerosis: The Role of Nrf2-Dependent Pathways.Antioxidants (Basel, Switzerland) · 2022Review
- Effects of Magnetite Nanoparticles and Static Magnetic Field on Neural Differentiation of Pluripotent Stem Cells.Stem cell reviews and reports · 2022Article
- Alcohol-Induced Neuroinflammatory Response and Mitochondrial Dysfunction on Aging and Alzheimer's Disease.Frontiers in behavioral neuroscience · 2021Review
- ROS systems are a new integrated network for sensing homeostasis and alarming stresses in organelle metabolic processes.Redox biology · 2020Review
- Chronic Alcohol Exposure Induces Aberrant Mitochondrial Morphology and Inhibits Respiratory Capacity in the Medial Prefrontal Cortex of Mice.Frontiers in neuroscience · 2020Article
- P2X7 Receptor Antagonism as a Potential Therapy in Amyotrophic Lateral Sclerosis.Frontiers in molecular neuroscience · 2020Review
- Coenzyme Q10 coadministration with diclofenac augmented impaired renal function in broiler chickens (Veterinary world · 2019Article
- Energy imbalance alters CaeLife · 2017Article
- PTPIP51 regulates mouse cardiac ischemia/reperfusion through mediating the mitochondria-SR junction.Scientific reports · 2017Article
- Riluzole But Not Melatonin Ameliorates Acute Motor Neuron Degeneration and Moderately Inhibits SOD1-Mediated Excitotoxicity Induced Disrupted Mitochondrial CaFrontiers in cellular neuroscience · 2016Article
- Selective vulnerability of motoneuron and perturbed mitochondrial calcium homeostasis in amyotrophic lateral sclerosis: implications for motoneurons specific calcium dysregulation.Molecular and cellular therapies · 2014Review
- Inhibition of West Nile virus by calbindin-D28k.PloS one · 2014Article
- Biology of mitochondria in neurodegenerative diseases.Progress in molecular biology and translational science · 2012Review
- Mitochondrial pathobiology in ALS.Journal of bioenergetics and biomembranes · 2011Review
- Links between electrophysiological and molecular pathology of amyotrophic lateral sclerosis.Integrative and comparative biology · 2011Review
- Konzo: from poverty, cassava, and cyanogen intake to toxico-nutritional neurological disease.PLoS neglected tropical diseases · 2011Review
- Persistent inward currents in spinal motoneurons: important for normal function but potentially harmful after spinal cord injury and in amyotrophic lateral sclerosis.Clinical neurophysiology : official journal of the International Federation of Clinical Neurophysiology · 2010Review
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
Motoneurones (MNs) are particularly affected by the inhibition of mitochondrial metabolism, which has been linked to their selective vulnerability during pathophysiological states like hypoxia and amyotrophic lateral sclerosis (ALS), a fatal neurodegenerative disorder. To elucidate underlying events, we used sodium cyanide (CN) as a pharmacological inhibitor of complex IV of the mitochondrial respiratory chain ('chemical hypoxia') and investigated the cellular response in vulnerable and resistant neurone types. Bath application of 2 mm CN activated TTX-insensitive Na+ conductances in vulnerable hypoglossal MNs, which depolarized these MNs by 10.2 +/- 1.1 mV and increased their action potential activity. This response was mimicked by sodium azide (2 mm) and largely prevented by preincubation with the antioxidants ascorbic acid (1 mm) and Trolox (750 microm), indicating an involvement of reactive oxygen species (ROS) in the activation mechanism. CN also elevated cytosolic [Ca2+] levels through (i) Ca2+ release from mitochondria-controlled stores, (ii) significant retardation of cytosolic Ca2+ clearance rates, even when cytosolic ATP levels were held constant during whole-cell recording, and (iii) secondary Ca2+ influx during elevated firing rates. Blocking mitochondrial ATP production additionally raised cytosolic Ca2+ levels and prolonged recovery of Ca2+ transients with a delay of 5-6 min. Comparative studies on hypoglossal MNs, facial MNs and dorsal vagal neurones suggested that CN responses were dominated by the activation of K+ conductances in resistant neurones, thus reducing excitability during mitochondrial inhibition. In summary, our observations therefore support a model where selective MN vulnerability results from a synergistic accumulation of risk factors, including low cytosolic Ca2+ buffering, strong mitochondrial impact on [Ca2+]i, and a mitochondria-controlled increase in electrical excitability during metabolic disturbances.
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