Synaptic mitochondria are critical for mobilization of reserve pool vesicles at Drosophila neuromuscular junctions.

By Patrik Verstreken, Cindy V. Ly, K. Venken, Tong-Wey Koh, Yi Zhou, Hugo J. Bellen. Neuron, 2005

866 citations recorded by the source corpus.

Subfields: Cell Biology, Cellular and Molecular Neuroscience, Molecular Biology

View Paper: https://www.semanticscholar.org/paper/65b146bf201bc8ff108aa476586d53cb660ed18f

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Cell Biology

1. D. C. Chan
2. Zu-Hang Sheng
3. Qian Cai
4. E. Holzbaur
5. P. Hollenbeck
6. J. Nunnari
7. W. Saxton
8. Alison E. Twelvetrees

In Cellular and Molecular Neuroscience

1. D. C. Chan
2. Oliver Kann
3. R. Kovács
4. R. Schwarzenbacher
5. J. Nunnari
6. Hsiuchen Chen
7. E. Bossy‐Wetzel

In Molecular Biology

1. D. C. Chan
2. Hsiuchen Chen
3. J. Nunnari
4. G. Perkins
5. E. Bossy‐Wetzel
6. R. Schwarzenbacher
7. A. B. Knott
8. Xiongwei Zhu

Citations in the corpus

• Glial Lipid Droplets and ROS Induced by Mitochondrial Defects Promote Neurodegeneration (2015, neutral): “In addition, retinal clones of Drp12, which encodes a protein involved in mitochondria fission (Verstreken et al., 2005), also do not result in LD accumulation (Figure Cell.”
• The axonal transport of mitochondria (2005, background): “Recent studies show that Drosophila mutants lacking the dynamin-related protein involved in mitochondrial fission fail to populate the distal axon with mitochondria (Verstreken et al., 2005), reminding us that the relationship between transport, location and biogenesis bears closer study.”
• Miro1 Is a Calcium Sensor for Glutamate Receptor-Dependent Localization of Mitochondria at Synapses (2009, neutral): “Mutations in proteins regulating mitochon- drial dynamics compromise synaptic function and plasticity (Li et al., 2004; Verstreken et al., 2005), and defective mitochondrial trafficking is implicated in neurological and neurodegenerative disease (Alexander et al., 2000; Baloh et al., 2007; Chan,…”
• Functions and dysfunctions of mitochondrial dynamics (2007, background): “Such distribution defects lead to reduced capacity for synaptic transmissio”
• Mitochondrial dynamics in health and disease: mechanisms and potential targets (2023, background): “174 Mutations in certain genes linked to familial PD have also highlighted the important role that mitochondrial dynamics play in this disorder.”
• Mitochondria and neuronal activity. (2007, background): “Nevertheless, a recent study in a Drosophila mutant lacking mitochondria in synapses suggests that mobilizing the reserve pool of synaptic vesicles depends on the presence of ATP rather than on mitochondrial Ca(2) buffering (214).”
• Mitochondrial fission factor Drp1 is essential for embryonic development and synapse formation in mice (2009, background): “, and neuronal function in fruitflies and cultured mammalian cell”
• Synaptic energy use and supply. (2012, neutral): “…to sleep), GluR1 subunits of AMPA receptors are present at a higher level and in a more phosphorylated state (consistent with an increased synaptic strength), synaptic currents and spine numbers increase, and evoked neuronal responses are larger (Vyazovskiy et al., 2008; Maret et al., 2011).”
• Mitochondrial fragmentation in neurodegeneration (2008, background): “melanogaster a Drp1 mutation prevented the mobilization of the neurotransmitter reserve poo”
• Mitochondrial fusion and fission in mammals. (2006, background): “For both Miro and Drp1 mutants, the neurons show only modest defects in Ca2+ buffering that are aggravated by prolonged, high-intensity activity (Guo et al. 2005, Verstreken et al. 2005).”