ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2006
Myosin light chain kinase is not a regulator of synaptic vesicle trafficking during repetitive exocytosis in cultured hippocampal neurons.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 39 citations in OpenAlex.
- Physiological implications of phase separation in vesicle organization and trafficking.BMC biology · 2026Review
- Importance of Full-Collapse Vesicle Exocytosis for Synaptic Fatigue-Resistance at Rat Fast and Slow Muscle Neuromuscular Junctions.International journal of molecular sciences · 2018Article
- Subdiffractional tracking of internalized molecules reveals heterogeneous motion states of synaptic vesicles.The Journal of cell biology · 2016Article
- Myosin accelerates synaptic vesicle recycling in the motor nerve endings.Doklady biological sciences : proceedings of the Academy of Sciences of the USSR, Biological sciences sections · 2016Article
- Article
- Myosin light chain kinase facilitates endocytosis of synaptic vesicles at hippocampal boutons.Journal of neurochemistry · 2016Article
- Non-muscle myosin II in disease: mechanisms and therapeutic opportunities.Disease models & mechanisms · 2015Review
- Myosin light chain kinase accelerates vesicle endocytosis at the calyx of Held synapse.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2014Article
- Synaptic bouton properties are tuned to best fit the prevailing firing pattern.Frontiers in computational neuroscience · 2014Article
- Reduced SNAP-25 alters short-term plasticity at developing glutamatergic synapses.EMBO reports · 2013Article
- Presynaptically localized cyclic GMP-dependent protein kinase 1 is a key determinant of spinal synaptic potentiation and pain hypersensitivity.PLoS biology · 2012Article
- Myosin VI contributes to synaptic transmission and development at the Drosophila neuromuscular junction.BMC neuroscience · 2011Article
- Post-tetanic increase in the fast-releasing synaptic vesicle pool at the expense of the slowly releasing pool.The Journal of general physiology · 2010Article
- Fos and Jun potentiate individual release sites and mobilize the reserve synaptic vesicle pool at the Drosophila larval motor synapse.Proceedings of the National Academy of Sciences of the United States of America · 2009Article
- F-actin and myosin II accelerate catecholamine release from chromaffin granules.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2009Article
- Activity-dependent coordination of presynaptic release probability and postsynaptic GluR2 abundance at single synapses.Proceedings of the National Academy of Sciences of the United States of America · 2008Article
- Presynaptic release probability and readily releasable pool size are regulated by two independent mechanisms during posttetanic potentiation at the calyx of Held synapse.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2008Article
- Synaptic vesicle mobility in mouse motor nerve terminals with and without synapsin.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2007Article
- Protein kinase inhibitors reduce GABA but not glutamate release in the nucleus accumbens.Neuropharmacology · 2007Article
- A delayed response enhancement during hippocampal presynaptic plasticity in mice.The Journal of physiology · 2007Article
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Authors and funding
2 authors at 2 institutions in 1 country.
Funding
Abstract
The mechanism by which synaptic vesicles (SVs) are recruited to the release site is poorly understood. One candidate mechanism for trafficking of SVs is the myosin-actin motor system. Myosin activity is modulated by myosin light chain kinase (MLCK), which in turn is activated by calmodulin. Ca(2+) signaling in presynaptic terminals, therefore, may serve to regulate SV mobility along actin filaments via MLCK. Previous studies in different types of synapses have supported such a hypothesis. Here, we further investigated the role of MLCK in neurotransmitter release at glutamatergic synapses in cultured hippocampal neurons by examining the effects of two MLCK inhibitors, 1-(5-iodonaphthalene-1-sulfonyl)-1H-hexahydro-1,4-diazepine.HCl (ML-7) and wortmannin. Bath application of ML-7 enhanced short-term depression of EPSCs to repetitive stimulation, whereas it reduced presynaptic release probability. However, ML-7 also inhibited action potential amplitude and voltage-gated Ca(2+) channel currents. These effects were not mimicked by wortmannin, suggesting that ML-7 was not specific to MLCK in hippocampal neurons. When SV exocytosis was directly triggered by a Ca(2+) ionophore, calcimycin, to bypass voltage-gated Ca(2+) channels, ML-7 had no effect on neurotransmitter release. Furthermore, when SV exocytosis elicited by electrical field stimulation was monitored by styryl dye, FM1-43 [N-(3-triethylammoniumpropyl)-4-(4-(dibutylamino)styryl)pyridinium dibromide], the unloading kinetics of the dye was not altered in the presence of wortmannin. These data indicate that MLCK is not a major regulator of presynaptic SV trafficking during repetitive exocytosis at hippocampal synapses.
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