Mitochondria – the kraken wakes!

  title={Mitochondria – the kraken wakes!},
  author={Richard J. Miller},
  journal={Trends in Neurosciences},
Roles of Na(+)-Ca2+ exchange and of mitochondria in the regulation of presynaptic Ca2+ and spontaneous glutamate release.
The results provide evidence for prominent roles of Na(+)-Ca2+ exchange and mitochondria in presynaptic Ca2+ regulation and spontaneous glutamate release.
Depolarization-Induced Mitochondrial Ca Accumulation in Sympathetic Neurons: Spatial and Temporal Characteristics
Measurements of depolarization-induced changes in intramitochondrialtotal Ca concentration obtained by x-ray microanalysis of rapidly frozen neurons from frog sympathetic ganglia demonstrate in situ Ca accumulation by mitochondria is robust, reversible, graded with stimulus strength and duration, and dependent on spatial location.
Mitochondria regulate TRPV4‐mediated release of ATP
Depolarised mitochondria switch TRPV4 signalling from relying on Ca2‐induced Ca2+ release at IP3 receptors to being independent of Ca2- influx and instead mediated by ATP release via pannexins.
Evolutionary and Functional Mitogenomics Associated With the Genetic Restoration of the Florida Panther
This work directly and indirectly assessed the presence of potential deleterious SNPs in the ND2 and ND5 genes in Florida panthers prior to and as a consequence of the introduction of Texas pumas.
Phenotypic characterization of PNPase knockdown in C. elegans
This document summarizes current capabilities, research and operational priorities, and plans for further studies that were established at the 2015 USGS workshop on quantitative hazard assessments of earthquake-triggered landsliding and liquefaction.
Reactive oxygen species trigger motoneuron death in non-cell-autonomous models of ALS through activation of c-Abl signaling
A sequence of events in which a toxic factor(s) released by ALS-expressing astrocytes rapidly induces hyper-excitability, which in turn increases calcium influx and affects mitochondrial structure and physiology is examined.
Changes in mitochondrial function are pivotal in neurodegenerative and psychiatric disorders: How important is BDNF?
It is argued that brain‐derived neurotrophic factor couples activity to changes in respiratory efficiency and these effects may be opposed by inflammatory cytokines, a key factor in neurodegenerative processes.
Exposure of cyclosporin A in whole blood, cerebral spinal fluid, and brain extracellular fluid dialysate in adults with traumatic brain injury.
CsA exposure characteristic differences exist for whole blood, CSF, and ECF dialysate in severe TBI patients when administered as a continuous intravenous infusion, and these exposure characteristics should be used for safer CsA dose optimization to achieve target C sA concentrations for neuroprotection in future TBI studies.


Ca2+ as a second messenger within mitochondria of the heart and other tissues.
Of the known second-messenger molecules that act within the cytosolic compartment of mammalian cells, it appears that only Ca2+ is transferred into the mitochondrial matrix.
Mitochondrial Implication in Accidental and Programmed Cell Death: Apoptosis and Necrosis
The notion that mitochondrial events control cell death has major implications for the development of death-inhibitory drugs.
Regulation of the intracellular free calcium concentration in single rat dorsal root ganglion neurones in vitro.
The relationship between the integrated ICa and the peak of the [Ca2+]i transient reached an asymptote at large Ca2+ loads indicating that Ca2(+)‐dependent processes became more efficient or that low‐affinity processes had been recruited.
The mitochondrial permeability transition.
The control of neuronal Ca2+ homeostasis
Mitochondrial calcium transport.
The permeability transition pore as a mitochondrial calcium release channel: A critical appraisal
The theoretical and experimental reasons why mitochondria need a fast, inducible Ca2+ release channel are discussed and the striking analogies between the mitochondrial permeability transition pore and the sarcoplasmic reticulum ryanodine receptor-Ca2+release channel are analyzed.