Role of myosin in neurotransmitter release: Functional studies at synapses formed in culture
References (63)
- et al.
Antibodies to synaptophysin interfere with transmitter secretion at neuromuscular synapses
Neuron
(1992) - et al.
Identification of myosin in isolated synaptic junctions
Brain Res
(1981) Actin and myosin in neurones: A first review
Biochimie
(1977)- et al.
Purification and structural analysis of myosin from brain and other non-muscle tissues
J Mol Biol
(1975) - et al.
Unconventional myosins
Curr Opin Cell Biol
(1992) - et al.
Two vesicle- associated membrane protein genes are differentially expressed in the rat central nervous system
J Biol Chem
(1989) Actin in the nervous system
Brain Res Rev
(1985)- et al.
Adenosinetriphosphatase activity in synaptic vesicle of rat brain
Biochem Pharmacol
(1965) - et al.
The calmodulin binding domain of chicken smooth muscle myosin light chain kinase contains a pseudosubstrate sequence
J Biol Chem
(1987) - et al.
Consensus sequences as substrate specificity determinants for protein kinases and protein phosphatases
J Biol Chem
(1991)
Inhibition of IgE-mediated histamine release by myosin light chain kinase inhibitors
Biochem Biophys Res Commun
Synaptic transmission between rat superior cervical ganglion neurons in dissociated cell cultures
Brain Res
Target regulation of neurotransmitter phenotype
Trends Neurosci
Immunocytochemical evidence for colocalization in neurite growth cones of actin and myosin and their relationship to cell-substratum adhesions
Dev Biol
Myosin II distribution in neurons is consistent with a role in growth cone motility but not synaptic vesicle mobilization
Neuron
Myosin II is involved in transmitter release at synapses formed between rat sympathetic neurons in culture
Neuron
Inhibition of Ca2+-dependent catecholamine release by myosin light chain kinase inhibitor, wortmannin, in adrenal chromaffin cells
Biochem Biophys Res Commun
Studies on rat sympathetic neurons developing in cell culture. III. Cholinergic transmission
Dev Biol
Characterization of a target-derived neuronal cholinergic differentiation factor
Neuron
Distribution of a gelsolin-like 74,000 mol wt protein in neural and endocrine tissues
Neuroscience
Botulinum neurotoxins are zinc protein
J Biol Chem
A synaptic vesicle membrane protein is conserved from mammals to Drosophila
Neuron
Contractile proteins in tissues originating in the neural crest
Neuroscience
Scinderin and chromaffin cell actin network dynamics during neurotransmitter release
J Physiol
A diffusible factor responsible for the determination of cholinergic functions in cultured sympathetic neurons
J Biol Chem
Identification and localization of synaptophysin, an integral membrane glycoprotein of Mr 38,000 characteristic of presynaptic vesicles
Cell
Partial purification and characterization of membrane-derived factor regulating neuro-transmitter phenotype expression
The cytoskeleton as a barrier to exocytosis in secretory cells
J Exp Biol
Syntaxin: A synaptic protein implicated in docking of synaptic vesicles at presynaptic active zones
Science
Mg2+-Ca2+-activated adenosine tri-phosphate system isolated from mamalian brain
Biochemistry
Actomyosin-like protein in brain
Science
Cited by (38)
Neurotensinergic augmentation of glutamate release at the perforant path-granule cell synapse in rat dentate gyrus: Roles of L-Type Ca<sup>2+</sup> channels, calmodulin and myosin light-chain kinase
2015, NeuropharmacologyCitation Excerpt :Second, increases in the function of presynaptic calmodulin enhances the readily releasable pool size at the calyx of Held synapse (Lee et al., 2010; Wu et al., 2009) and application of the calmodulin antagonist, calmidazolium, blocks nicotine-induced increase in the size of the readily releasable pool at dopamine terminals (Turner, 2004). Third, myosin and MLCK have been demonstrated to be involved in the mobilization of synaptic vesicles at a variety of synapses (Mochida, 1995; Mochida et al., 1994) including the hippocampal synapses (Ryan, 1999). Because the hippocampal synapses are capable of multivesicular release (Christie and Jahr, 2006; Oertner et al., 2002; Tong and Jahr, 1994) and application of estradiol (Smejkalova and Woolley, 2010) or LTP-induction protocols (Bender et al., 2009) facilitates multivesicular release, it is rational to hypothesize that NT facilitates glutamate release by increasing multivesicular release.
Tomosyn inhibits synaptotagmin-1-mediated step of Ca<sup>2+</sup>-dependent neurotransmitter release through its N-terminal WD40 repeats
2010, Journal of Biological ChemistryCitation Excerpt :Postnatal day 7 Wistar ST rats were decapitated under diethyl ether anesthesia according to the guidelines of the Physiological Society of Japan. Isolated SCG neurons were maintained in culture for 5–6 weeks as described (43, 44). In brief, SCGs were dissected, desheathed, and incubated with collagenase (0.5 mg/ml; Worthington) in L-15 (Invitrogen) at 37 °C for 10 min.
Friends and foes in synaptic transmission: the role of tomosyn in vesicle priming
2009, Trends in NeurosciencesCitation Excerpt :Moreover, the yeast tomosyn homologs Sro7/77 were shown to bind to yeast Myo1p and Myo2p (equivalent to non-muscle myosin II and myosin V in mammalian cells) [49]. Note that myosin II and myosin V have recently been suggested to be involved in a post-docking step in chromaffin cells and neurons [52–58]. It is, therefore, possible that the N-terminal domain of tomosyn interacts with cytoskeletal proteins and modulates exocytosis through these interactions; one possible scenario might be that the N-terminal domain of tomosyn inhibits exocytosis by interfering with the syntaxin–myosin interaction, which is important for exocytosis [56].
Dynamin and activity regulate synaptic vesicle recycling in sympathetic neurons
2009, Journal of Biological ChemistryCitation Excerpt :To reach the final concentration it takes a few minutes after bath superfusion was stopped (31). Before recording EPSPs at 20 min after the Dynasore application, cultured SCG neurons showed no spontaneous synaptic activity (32), suggesting that reduction of SVs in the RRP with the treatment is unlikely. Error bars shown in the text and figures represent mean ± S.E.
Immunopharmacology - Antibodies for specific modulation of proteins involved in neuronal function
2005, Journal of Neuroscience MethodsNCAM 180 acting via a conserved C-terminal domain and MLCK is essential for effective transmission with repetitive stimulation
2005, NeuronCitation Excerpt :We previously observed that transmission failures similar to those observed in NCAM null or 180 isoform null NMJs could be produced by the MLCK inhibitor ML-9 at concentrations considered specific for MLCK (Polo-Parada et al., 2001; Polo-Parada et al., 2004). Previous studies have shown that inhibiting the action of MLCK by drugs such as ML-9 (Ryan, 1999) or specific blocking peptides (Mochida et al., 1994; Mochida, 1995) interferes with normal neural transmission. However, because of potential lack of specificity of ML-9, we used the peptide carrier method to introduce an inhibitory peptide known to block MLCK (Kemp et al., 1987).