45 Citations
Roles of Na(+)-Ca2+ exchange and of mitochondria in the regulation of presynaptic Ca2+ and spontaneous glutamate release.
- BiologyPhilosophical transactions of the Royal Society of London. Series B, Biological sciences
- 1999
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
- BiologyThe Journal of Neuroscience
- 1999
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
- BiologyBritish journal of pharmacology
- 2021
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
- BiologyThe Journal of heredity
- 2017
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
- Biology
- 2015
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.
Intracellular zinc is a critical intermediate in the excitotoxic cascade
- BiologyNeurobiology of Disease
- 2015
Reactive oxygen species trigger motoneuron death in non-cell-autonomous models of ALS through activation of c-Abl signaling
- BiologyFront. Cell. Neurosci.
- 2015
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?
- Biology, PsychologyBritish journal of pharmacology
- 2014
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.
- Medicine, BiologyJournal of neurotrauma
- 2013
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.
References
SHOWING 1-10 OF 21 REFERENCES
Ca2+ as a second messenger within mitochondria of the heart and other tissues.
- Biology, Computer ScienceAnnual review of physiology
- 1990
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
- BiologyJournal of bioenergetics and biomembranes
- 1997
The notion that mitochondrial events control cell death has major implications for the development of death-inhibitory drugs.
Bright and dark sides of nitric oxide in ischemic brain injury
- BiologyTrends in Neurosciences
- 1997
Regulation of the intracellular free calcium concentration in single rat dorsal root ganglion neurones in vitro.
- BiologyThe Journal of physiology
- 1990
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.
Why are mitochondria involved in apoptosis? Permeability transition pores and apoptosis as selective mechanisms to eliminate superoxide‐producing mitochondria and cell
- BiologyFEBS letters
- 1996
The permeability transition pore as a mitochondrial calcium release channel: A critical appraisal
- BiologyJournal of bioenergetics and biomembranes
- 1996
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.