ArticleBiophysical journal2013
Mitochondrial free Ca²⁺ levels and their effects on energy metabolism in Drosophila motor nerve terminals.
Article in Biophysical journal, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers, 1 of them a synthesis that pooled it.
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Who cites it
34 citing papers in PubMed, 1 synthesis or guideline pooled it, 65 citations in OpenAlex.
- The Intersection of Mitophagy and Autism Spectrum Disorder: A Systematic Review.International journal of molecular sciences · 2025Pooled it
- Ratiometric Imaging for Quantification of Elevated CaACS chemical neuroscience · 2025Article
- Loss of mitochondrial CaCell communication and signaling : CCS · 2024Article
- ATF4-dependent increase in mitochondrial-endoplasmic reticulum tethering following OPA1 deletion in skeletal muscle.Journal of cellular physiology · 2024Article
- Diphenyl Diselenide Attenuates Mitochondrial Damage During Initial Hypoxia and Enhances Resistance to Recurrent Hypoxia.Neurotoxicity research · 2024Article
- Mitochondrial phosphagen kinases support the volatile power demands of motor nerve terminals.The Journal of physiology · 2023Article
- Targeted proteomic analysis reveals that crocodile oil from Crocodylus siamensis may enhance hepatic energy metabolism in rats.Experimental animals · 2023Article
- Treatment of Autism Spectrum Disorders by Mitochondrial-targeted Drug: Future of Neurological Diseases Therapeutics.Current neuropharmacology · 2023Review
- Mitochondrial calcium cycling in neuronal function and neurodegeneration.Frontiers in cell and developmental biology · 2023Review
- Loss of Activity-Induced Mitochondrial ATP Production Underlies the Synaptic Defects in aThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2022Article
- Developmental shift to mitochondrial respiration for energetic support of sustained transmission during maturation at the calyx of Held.Journal of neurophysiology · 2021Article
- Regulation of longevity by depolarization-induced activation of PLC-β-IPProceedings of the National Academy of Sciences of the United States of America · 2021Article
- Influence of Mpv17 on Hair-Cell Mitochondrial Homeostasis, Synapse Integrity, and Vulnerability to Damage in the Zebrafish Lateral Line.Frontiers in cellular neuroscience · 2021Article
- Mitochondria: The Retina's Achilles' Heel in AMD.Advances in experimental medicine and biology · 2021Article
- Calcium signaling: breast cancer's approach to manipulation of cellular circuitry.Biophysical reviews · 2020Review
- The Role of Mitochondrial Calcium Homeostasis in Alzheimer's and Related Diseases.International journal of molecular sciences · 2020Review
- Altered Outer Hair Cell Mitochondrial and Subsurface Cisternae Connectomics Are Candidate Mechanisms for Hearing Loss in Mice.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2020Article
- Regulation of cellular senescence by eukaryotic members of the FAH superfamily - A role in calcium homeostasis?Mechanisms of ageing and development · 2020Review
- Precipitation of Inorganic Salts in Mitochondrial Matrix.Membranes · 2020Article
- Why don't mice lacking the mitochondrial CaThe Journal of physiology · 2020Review
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Mitochondrial Ca²⁺ uptake exerts dual effects on mitochondria. Ca²⁺ accumulation in the mitochondrial matrix dissipates membrane potential (ΔΨm), but Ca²⁺ binding of the intramitochondrial enzymes accelerates oxidative phosphorylation, leading to mitochondrial hyperpolarization. The levels of matrix free Ca²⁺ ([Ca²⁺]m) that trigger these metabolic responses in mitochondria in nerve terminals have not been determined. Here, we estimated [Ca²⁺]m in motor neuron terminals of Drosophila larvae using two methods: the relative responses of two chemical Ca²⁺ indicators with a 20-fold difference in Ca²⁺ affinity (rhod-FF and rhod-5N), and the response of a low-affinity, genetically encoded ratiometric Ca²⁺ indicator (D4cpv) calibrated against known Ca²⁺ levels. Matrix pH (pHm) and ΔΨm were monitored using ratiometric pericam and tetramethylrhodamine ethyl ester probe, respectively, to determine when mitochondrial energy metabolism was elevated. At rest, [Ca²⁺]m was 0.22 ± 0.04 μM, but it rose to ~26 μM (24.3 ± 3.4 μM with rhod-FF/rhod-5N and 27.0 ± 2.6 μM with D4cpv) when the axon fired close to its endogenous frequency for only 2 s. This elevation in [Ca²⁺]m coincided with a rapid elevation in pHm and was followed by an after-stimulus ΔΨm hyperpolarization. However, pHm decreased and no ΔΨm hyperpolarization was observed in response to lower levels of [Ca²⁺]m, up to 13.1 μM. These data indicate that surprisingly high levels of [Ca²⁺]m are required to stimulate presynaptic mitochondrial energy metabolism.
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