ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2013
Myosin II regulates activity dependent compensatory endocytosis at central synapses.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 38 citations in OpenAlex.
- Cisplatin-Induced APE2 Overexpression Disrupts MYH9 Function and Causes Hearing Loss.Cancer research communications · 2025Article
- Thick Ascending Limb Specific Inactivation of Myh9 and Myh10 Myosin Motors Results in Progressive Kidney Disease and Drives Sex-specific Cellular Adaptation in the Distal Nephron and Collecting Duct.Function (Oxford, England) · 2025Article
- Single-vesicle imaging reveals actin-dependent spatial restriction of vesicles at the active zone, essential for sustained transmission.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Actin cytoskeleton and associated myosin motors within the renal epithelium.American journal of physiology. Renal physiology · 2024Review
- Article
- Presynapses contain distinct actin nanostructures.The Journal of cell biology · 2023Article
- Isoform selectivities of novel 4-hydroxycoumarin imines as inhibitors of myosin II.European journal of medicinal chemistry · 2023Article
- Pseudokinase NRP1 facilitates endocytosis of transferrin in the African trypanosome.Scientific reports · 2022Article
- Multiple Roles of Actin in Exo- and Endocytosis.Frontiers in synaptic neuroscience · 2022Review
- Conditional Myh9 and Myh10 inactivation in adult mouse renal epithelium results in progressive kidney disease.JCI insight · 2020Article
- Synthesis and Evaluation of 4-Hydroxycoumarin Imines as Inhibitors of Class II Myosins.Journal of medicinal chemistry · 2020Article
- Review
- The Myosin Family of Mechanoenzymes: From Mechanisms to Therapeutic Approaches.Annual review of biochemistry · 2020Review
- Blebbistatin, a Myosin II Inhibitor, Exerts Antidepressant-Like Activity and Suppresses Detrusor Overactivity in an Animal Model of Depression Coexisting with Overactive Bladder.Neurotoxicity research · 2019Article
- Article
- Nonmuscle myosin 2 proteins encoded byPhysiological reports · 2017Article
- Activity-Dependence of Synaptic Vesicle Dynamics.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2017Article
- Optical magnetic detection of single-neuron action potentials using quantum defects in diamond.Proceedings of the National Academy of Sciences of the United States of America · 2016Article
- The calyx of Held in the auditory system: Structure, function, and development.Hearing research · 2016Review
- Myosin light chain kinase facilitates endocytosis of synaptic vesicles at hippocampal boutons.Journal of neurochemistry · 2016Article
Corrections and comments
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Authors and funding
4 authors at 3 institutions in 2 countries.
Funding
Abstract
Recent evidence suggests that endocytosis, not exocytosis, can be rate limiting for neurotransmitter release at excitatory CNS synapses during sustained activity and therefore may be a principal determinant of synaptic fatigue. At low stimulation frequencies, the probability of synaptic release is linked to the probability of synaptic retrieval such that evoked release results in proportional retrieval even for release of single synaptic vesicles. The exact mechanism by which the retrieval rates are coupled to release rates, known as compensatory endocytosis, remains unknown. Here we show that inactivation of presynaptic myosin II (MII) decreases the probability of synaptic retrieval. To be able to differentiate between the presynaptic and postsynaptic functions of MII, we developed a live cell substrate patterning technique to create defined neural circuits composed of small numbers of embryonic mouse hippocampal neurons and physically isolated from the surrounding culture. Acute application of blebbistatin to inactivate MII in circuits strongly inhibited evoked release but not spontaneous release. In circuits incorporating both control and MIIB knock-out cells, loss of presynaptic MIIB function correlated with a large decrease in the amplitude of evoked release. Using activity-dependent markers FM1-43 and horseradish peroxidase, we found that MII inactivation greatly slowed vesicular replenishment of the recycling pool but did not impede synaptic release. These results indicate that MII-driven tension or actin dynamics regulate the major pathway for synaptic vesicle retrieval. Changes in retrieval rates determine the size of the recycling pool. The resulting effect on release rates, in turn, brings about changes in synaptic strength.
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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.