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J Neurosci
2010 Mar 10;3010:3555-66. doi: 10.1523/JNEUROSCI.4551-09.2010.
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Activity-dependent regulation of mitochondrial motility by calcium and Na/K-ATPase at nodes of Ranvier of myelinated nerves.
Zhang CL, Ho PL, Kintner DB, Sun D, Chiu SY.
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The node of Ranvier is a tiny segment of a myelinated fiber with various types of specializations adapted for generation of high-speed nerve impulses. It is ionically specialized with respect to ion channel segregation and ionic fluxes, and metabolically specialized in ionic pump expression and mitochondrial density augmentation. This report examines the interplay of three important parameters (calcium fluxes, Na pumps, mitochondrial motility) at nodes of Ranvier in frog during normal nerve activity. First, we used calcium dyes to resolve a highly localized elevation in axonal calcium at a node of Ranvier during action potentials, and showed that this calcium elevation retards mitochondrial motility during nerve impulses. Second, we found, surprisingly, that physiologic activation of the Na pumps retards mitochondrial motility. Blocking Na pumps alone greatly prevents action potentials from retarding mitochondrial motility, which reveals that mitochondrial motility is coupled to Na/K-ATPase. In conclusion, we suggest that during normal nerve activity, Ca elevation and activation of Na/K-ATPase act, possibly in a synergistic manner, to recruit mitochondria to a node of Ranvier to match metabolic needs.
Andrews,
Mitochondrial dysfunction plays a key role in progressive axonal loss in Multiple Sclerosis.
2005, Pubmed
Andrews,
Mitochondrial dysfunction plays a key role in progressive axonal loss in Multiple Sclerosis.
2005,
Pubmed Andrews,
Increased axonal mitochondrial activity as an adaptation to myelin deficiency in the Shiverer mouse.
2006,
Pubmed Baloh,
Altered axonal mitochondrial transport in the pathogenesis of Charcot-Marie-Tooth disease from mitofusin 2 mutations.
2007,
Pubmed Baloh,
Mitochondrial dynamics and peripheral neuropathy.
2008,
Pubmed Baron,
CGP37157 modulates mitochondrial Ca2+ homeostasis in cultured rat dorsal root ganglion neurons.
1997,
Pubmed Bechtold,
Axonal protection in experimental autoimmune neuritis by the sodium channel blocking agent flecainide.
2005,
Pubmed Brough,
Agonist-induced regulation of mitochondrial and endoplasmic reticulum motility.
2005,
Pubmed Cai,
Moving or stopping mitochondria: Miro as a traffic cop by sensing calcium.
2009,
Pubmed Chan,
Mitochondrial dynamics in disease.
2007,
Pubmed Chiu,
Potassium channels in nodal and internodal axonal membrane of mammalian myelinated fibres.
1980,
Pubmed Chiu,
Asymmetry currents in the mammalian myelinated nerve.
1980,
Pubmed Cooper,
The movement of optically detectable organelles in myelinated axons of Xenopus laevis.
1974,
Pubmed
,
Xenbase Cox,
Selectivity of inhibition of Na(+)-Ca2+ exchange of heart mitochondria by benzothiazepine CGP-37157.
1993,
Pubmed Craner,
Co-localization of sodium channel Nav1.6 and the sodium-calcium exchanger at sites of axonal injury in the spinal cord in EAE.
2004,
Pubmed David,
Mitochondrial clearance of cytosolic Ca(2+) in stimulated lizard motor nerve terminals proceeds without progressive elevation of mitochondrial matrix [Ca(2+)].
1999,
Pubmed Detmer,
Functions and dysfunctions of mitochondrial dynamics.
2007,
Pubmed Dutta,
Mitochondrial dysfunction as a cause of axonal degeneration in multiple sclerosis patients.
2006,
Pubmed Edgar,
Distribution of mitochondria along small-diameter myelinated central nervous system axons.
2008,
Pubmed Einheber,
Disrupted axo-glial junctions result in accumulation of abnormal mitochondria at nodes of ranvier.
2006,
Pubmed Fabricius,
Axoplasmic organelles at nodes of Ranvier. II. Occurrence and distribution in large myelinated spinal cord axons of the adult cat.
1993,
Pubmed Gordon,
Electrogenic pump (Na+/K(+)-ATPase) activity in rat optic nerve.
1990,
Pubmed Hollenbeck,
The axonal transport of mitochondria.
2005,
Pubmed Hom,
Thapsigargin induces biphasic fragmentation of mitochondria through calcium-mediated mitochondrial fission and apoptosis.
2007,
Pubmed Kaji,
Effect of digitalis on central demyelinative conduction block in vivo.
1989,
Pubmed Kennedy,
Glucose generates sub-plasma membrane ATP microdomains in single islet beta-cells. Potential role for strategically located mitochondria.
1999,
Pubmed Kolikova,
Calcium-dependent trapping of mitochondria near plasma membrane in stimulated astrocytes.
2006,
Pubmed Macaskill,
Miro1 is a calcium sensor for glutamate receptor-dependent localization of mitochondria at synapses.
2009,
Pubmed Mahad,
Mitochondrial changes within axons in multiple sclerosis.
2009,
Pubmed Mahad,
Mitochondrial defects in acute multiple sclerosis lesions.
2008,
Pubmed Mima,
Short-term high-frequency transcutaneous electrical nerve stimulation decreases human motor cortex excitability.
2004,
Pubmed Mironov,
ADP regulates movements of mitochondria in neurons.
2007,
Pubmed Mironov,
Spontaneous and evoked neuronal activities regulate movements of single neuronal mitochondria.
2006,
Pubmed Misgeld,
Imaging axonal transport of mitochondria in vivo.
2007,
Pubmed Pitter,
Mitochondria respond to Ca2+ already in the submicromolar range: correlation with redox state.
2002,
Pubmed Poliak,
The local differentiation of myelinated axons at nodes of Ranvier.
2003,
Pubmed Quintana,
Sustained activity of calcium release-activated calcium channels requires translocation of mitochondria to the plasma membrane.
2006,
Pubmed Saotome,
Bidirectional Ca2+-dependent control of mitochondrial dynamics by the Miro GTPase.
2008,
Pubmed Smith,
The pathophysiology of multiple sclerosis: the mechanisms underlying the production of symptoms and the natural history of the disease.
1999,
Pubmed Smith,
Spontaneous and mechanically evoked activity due to central demyelinating lesion.
1980,
Pubmed Stys,
General mechanisms of axonal damage and its prevention.
2005,
Pubmed Sun,
N-type calcium channels and their regulation by GABAB receptors in axons of neonatal rat optic nerve.
1999,
Pubmed Thastrup,
Thapsigargin, a tumor promoter, discharges intracellular Ca2+ stores by specific inhibition of the endoplasmic reticulum Ca2(+)-ATPase.
1990,
Pubmed Verbny,
Coupling of calcium homeostasis to axonal sodium in axons of mouse optic nerve.
2002,
Pubmed Wang,
The mechanism of Ca2+ -dependent regulation of kinesin-mediated mitochondrial motility.
2009,
Pubmed Waxman,
Axonal dysfunction in chronic multiple sclerosis: meltdown in the membrane.
2008,
Pubmed Waxman,
Axonal conduction and injury in multiple sclerosis: the role of sodium channels.
2006,
Pubmed Yang,
Ca2+ influx-independent synaptic potentiation mediated by mitochondrial Na(+)-Ca2+ exchanger and protein kinase C.
2003,
Pubmed
,
Xenbase Yi,
Control of mitochondrial motility and distribution by the calcium signal: a homeostatic circuit.
2004,
Pubmed Young,
Imaging correlates of decreased axonal Na+/K+ ATPase in chronic multiple sclerosis lesions.
2008,
Pubmed Zhang,
Nicotinic acetylcholine receptors in mouse and rat optic nerves.
2004,
Pubmed Zhang,
Action potentials induce uniform calcium influx in mammalian myelinated optic nerves.
2006,
Pubmed
