ReviewJournal of bioenergetics and biomembranes2011
Mitochondria in motor nerve terminals: function in health and in mutant superoxide dismutase 1 mouse models of familial ALS.
Review in Journal of bioenergetics and biomembranes, 2011. 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
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
15 citing papers in PubMed, 25 citations in OpenAlex.
- Monitoring presynaptic calcium dynamics with membrane-impermeant fluorescent indicators in motor nerve endings.Biophysical reviews · 2025Review
- Targeting mitochondrial CaThe Journal of physiology · 2024Review
- Restoring Mitochondrial Function and Muscle Satellite Cell Signaling: Remedies against Age-Related Sarcopenia.Biomolecules · 2024Review
- Structure and Function of the Mammalian Neuromuscular Junction.Comprehensive Physiology · 2022Article
- Central and Peripheral Neuromuscular Adaptations to Ageing.Journal of clinical medicine · 2020Review
- CRISPR/Cas9: a powerful genetic engineering tool for establishing large animal models of neurodegenerative diseases.Molecular neurodegeneration · 2015Review
- Purkinje neuron Ca2+ influx reduction rescues ataxia in SCA28 model.The Journal of clinical investigation · 2015Article
- Elevated mRNA-levels of distinct mitochondrial and plasma membrane Ca(2+) transporters in individual hypoglossal motor neurons of endstage SOD1 transgenic mice.Frontiers in cellular neuroscience · 2014Article
- The Neuromuscular Junction: Aging at the Crossroad between Nerves and Muscle.Frontiers in aging neuroscience · 2014Review
- 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
- SOD2 in mitochondrial dysfunction and neurodegeneration.Free radical biology & medicine · 2013Review
- Characterization of early pathogenesis in the SOD1(G93A) mouse model of ALS: part I, background and methods.Brain and behavior · 2013Article
- Molecular signatures of amyotrophic lateral sclerosis disease progression in hind and forelimb muscles of an SOD1(G93A) mouse model.Antioxidants & redox signaling · 2012Article
- Mitochondria, calcium-dependent neuronal death and neurodegenerative disease.Pflugers Archiv : European journal of physiology · 2012Review
- Introduction to the minireviews series on mitochondrial matters in amyotrophic lateral sclerosis, Lou Gehrig’s disease.Journal of bioenergetics and biomembranes · 2011Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Mitochondria contribute to neuronal function not only via their ability to generate ATP, but also via their ability to buffer large Ca(2+) loads. This review summarizes evidence that mitochondrial Ca(2+) sequestration is especially important for sustaining the function of vertebrate motor nerve terminals during repetitive stimulation. Motor terminal mitochondria can sequester large amounts of Ca(2+) because they have mechanisms for limiting both the mitochondrial depolarization and the increase in matrix free [Ca(2+)] associated with Ca(2+) influx. In mice expressing mutations of human superoxide dismutase -1 (SOD1) that cause some cases of familial amyotrophic lateral sclerosis (fALS), motor terminals degenerate well before the death of motor neuron cell bodies. This review presents evidence for early and progressive mitochondrial dysfunction in motor terminals of mutant SOD1 mice (G93A, G85R). This dysfunction would impair mitochondrial ability to sequester stimulation-associated Ca(2+) loads, and thus likely contributes to the early degeneration of motor terminals.
Indexed as
Identifiers
What OpenQuestion holds
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.