ArticleThe Journal of physiology2003
Stimulation-induced mitochondrial [Ca2+] elevations in mouse motor terminals: comparison of wild-type with SOD1-G93A.
Article in The Journal of physiology, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
15 citing papers in PubMed, 31 citations in OpenAlex.
- Mitochondrial Mutations Can Alter Neuromuscular Transmission in Congenital Myasthenic Syndrome and Mitochondrial Disease.International journal of molecular sciences · 2023Review
- Structure and Function of the Mammalian Neuromuscular Junction.Comprehensive Physiology · 2022Article
- Dysregulated mitochondrial CaArchives of biochemistry and biophysics · 2019Review
- Dysfunctional mitochondrial Ca(2+) handling in mutant SOD1 mouse models of fALS: integration of findings from motor neuron somata and motor terminals.Frontiers in cellular neuroscience · 2014Article
- Selective mitochondrial Ca2+ uptake deficit in disease endstage vulnerable motoneurons of the SOD1G93A mouse model of amyotrophic lateral sclerosis.The Journal of physiology · 2013Article
- Early changes of neuromuscular transmission in the SOD1(G93A) mice model of ALS start long before motor symptoms onset.PloS one · 2013Article
- Calcium dependence of damage to mouse motor nerve terminals following oxygen/glucose deprivation.Experimental neurology · 2012Article
- Mitochondrial dynamics and bioenergetic dysfunction is associated with synaptic alterations in mutant SOD1 motor neurons.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2012Article
- Mitochondrial dysfunction in familial amyotrophic lateral sclerosis.Journal of bioenergetics and biomembranes · 2011Review
- Mitochondria in motor nerve terminals: function in health and in mutant superoxide dismutase 1 mouse models of familial ALS.Journal of bioenergetics and biomembranes · 2011Review
- Repetitive nerve stimulation transiently opens the mitochondrial permeability transition pore in motor nerve terminals of symptomatic mutant SOD1 mice.Neurobiology of disease · 2011Article
- Olesoxime (TRO19622): A Novel Mitochondrial-Targeted Neuroprotective Compound.Pharmaceuticals (Basel, Switzerland) · 2010Review
- Hyperactive intracellular calcium signaling associated with localized mitochondrial defects in skeletal muscle of an animal model of amyotrophic lateral sclerosis.The Journal of biological chemistry · 2010Article
- Early vulnerability to ischemia/reperfusion injury in motor terminals innervating fast muscles of SOD1-G93A mice.Experimental neurology · 2007Article
- Mitochondrial involvement in amyotrophic lateral sclerosis: trigger or target?Molecular neurobiology · 2006Review
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Changes in mitochondrial matrix [Ca2+] evoked by trains of action potentials were studied in levator auris longus motor terminals using Ca2+-sensitive fluorescent indicator dyes (rhod-2, rhod-5F). During a 2500 impulse 50 Hz train, mitochondrial [Ca2+] in most wild-type terminals increased within 5-10 s to a plateau level that was sustained until stimulation ended. This plateau was not due to dye saturation, but rather reflects a powerful buffering system within the mitochondrial matrix. The amplitude of this plateau was similar for stimulation frequencies in the range 15-100 Hz. Plateau amplitude was sensitive to temperature, with no detectable stimulation-induced increase in fluorescence at temperatures below 17 degrees C, and increasing magnitudes as temperature was increased to near-physiological levels (38 degrees C). When stimulation ended, mitochondrial [Ca2+] decayed slowly back to prestimulation levels over a time course of hundreds of seconds. Similar measurements were also made in motor terminals of mice expressing the G93A mutation of human superoxide dismutase 1 (SOD1-G93A). In mice > 100 days old, all of whom exhibited hindlimb paralysis, some terminals continued to show wild-type mitochondrial [Ca2+] responses, but in other terminals mitochondrial [Ca2+] did not plateau, but rather continued to increase throughout most of the stimulus train. Thus mechanism(s) that limit stimulation-induced increases in mitochondrial [Ca2+] may be compromised in some SOD1-G93A terminals.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.