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19 results for “Synaptic vesicles”
Unique dynamics and exocytosis properties of GABAergic synaptic vesicles revealed by three-dimensional single vesicle tracking
<p>This data set includes x, y, and z trajectories of all GABAergic synaptic vesicles that we used for the study. These GABAergic synaptic vesicles in inhibitory presynaptic terminals of living primary hippocampal neurons were labeled by single quantum dots (QDs) conjugated with anti-VGAT antibody under electrical stimulation, and were tracked three-dimensionally by using a dual-focus imaging in real-time. Each trajectory data indicates x, y, and z positions (nanometer-scale) over time from the start of imaging to the moment of vesicle fusion. The electrical stimulation to the neurons was applied for 120 s, starting from 20 s.</p>
Dataset related to article "Glia-to-neuron transfer of miRNAs via extracellular vesicles: a new mechanism underlying inflammation-induced synaptic alterations"
<p>This record contains raw data related to article "Glia-to-neuron transfer of miRNAs via extracellular vesicles: a new mechanism underlying inflammation-induced synaptic alterations"</p> <p>Recent evidence indicates synaptic dysfunction as an early mechanism affected in neuroinflammatory diseases, such as multiple sclerosis, which are characterized by chronic microglia activation. However, the mode(s) of action of reactive microglia in causing synaptic defects are not fully understood. In this study, we show that inflammatory microglia produce extracellular vesicles (EVs) which are enriched in a set of miRNAs that regulate the expression of key synaptic proteins. Among them, miR-146a-5p, a microglia-specific miRNA not present in hippocampal neurons, controls the expression of presynaptic synaptotagmin1 (Syt1) and postsynaptic neuroligin1 (Nlg1), an adhesion protein which play a crucial role in dendritic spine formation and synaptic stability. Using a Renilla-based sensor, we provide formal proof that inflammatory EVs transfer their miR-146a-5p cargo to neuron. By western blot and immunofluorescence analysis we show that vesicular miR-146a-5p suppresses Syt1 and Nlg1 expression in receiving neurons. Microglia-to-neuron miR-146a-5p transfer and Syt1 and Nlg1 downregulation do not occur when EV-neuron contact is inhibited by cloaking vesicular phosphatidylserine residues and when neurons are exposed to EVs either depleted of miR-146a-5p, produced by pro-regenerative microglia, or storing inactive miR-146a-5p, produced by cells transfected with an anti-miR-146a-5p. Morphological analysis reveals that prolonged exposure to inflammatory EVs leads to significant decrease in dendritic spine density in hippocampal neurons in vivo and in primary culture, which is rescued in vitro by transfection of a miR-insensitive Nlg1 form. Dendritic spine loss is accompanied by a decrease in the density and strength of excitatory synapses, as indicated by reduced mEPSC frequency and amplitude. These findings link inflammatory microglia and enhanced EV production to loss of excitatory synapses, uncovering a previously unrecognized role for microglia-enriched miRNAs, released in association to EVs, in silencing of key synaptic genes.</p>
Dopamine transporter and synaptic vesicle sorting defects underlie auxilin-associated Parkinson's disease
<p>Auxilin participates in clathrin uncoating to facilitate presynaptic endocytosis. Loss-of-function mutations of auxilin (<em>PARK19</em>) cause Parkinson’s disease. Using auxilin KO mice, Vidyadhara et al. (2023) show that synaptic vesicle sorting deficits, cytoplasmic dopamine accumulation, dopamine transporter mistrafficking, and synaptic autophagic overload may lead to pathogenesis of Parkinson’s disease in <em>PARK19</em> patients. This file contains the data set used to generate all the main figures.</p>
Data from: Kif1a and intact microtubules maintain synaptic-vesicle populations at ribbon synapses in zebrafish hair cells
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Synaptic vesicle glycoprotein 2C enhances vesicular storage of dopamine and counters dopaminergic toxicity
<p>Dopaminergic neurons of the substantia nigra exist in a persistent state of vulnerability resulting from high baseline oxidative stress, high energy demand, and broad unmyelinated axonal arborizations. Impairments in the storage of dopamine compound this stress due to cytosolic reactions that transform the vital neurotransmitter into an endogenous neurotoxicant, and this toxicity is thought to contribute to the dopamine neuron degeneration that occurs Parkinson's disease. We have previously identified synaptic vesicle glycoprotein 2C (SV2C) as a modifier of vesicular dopamine function, demonstrating that genetic ablation of SV2C in mice results in decreased dopamine content and evoked dopamine release in the striatum. Here, we adapted a previously published in vitro assay utilizing false fluorescent neurotransmitter 206 (FFN206) to visualize how SV2C regulates vesicular dopamine dynamics and identified that SV2C promotes the uptake and retention of FFN206 within vesicles. In addition, we present data indicating that SV2C enhances the retention of dopamine in the vesicular compartment with radiolabeled dopamine in vesicles isolated from immortalized cells and from mouse brain. Further, we demonstrate that SV2C enhances the ability of vesicles to store the neurotoxicant 1-methyl-4-phenylpyridinium (MPP+) and that genetic ablation of SV2C results in enhanced 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced vulnerability in mice. Together, these findings establish that SV2C functions to enhance storage of dopamine and toxicants and helps maintain the integrity of dopaminergic neurons.</p>
All-atom molecular dynamics simulations of synaptic vesicle fusion I: a glimpse at the primed Synaptotagmin-SNARE-complexin complex
<p>Synaptic vesicles are primed into a state that is ready for fast neurotransmitter release upon Ca<sup>2+</sup>-binding to Syt1. This state likely includes trans-SNARE complexes between the vesicle and plasma membranes that are bound to Syt1 and complexins. However, the nature of this state and the steps leading to membrane fusion are unclear, in part because of the difficulty of studying this dynamic process experimentally. To shed light into these questions, we performed all-atom molecular dynamics simulations of systems containing trans-SNARE complexes between two flat bilayers or a vesicle and a flat bilayer with or without fragments of Syt1 and/or complexin-1. Our results need to be interpreted with caution because of the limited simulation times and the absence of key components, but suggest mechanistic features that may control release and help visualize potential states of the primed Syt1-SNARE-complexin-1 complex. In particular, the simulations suggest that SNAREs alone induce formation of extended membrane-membrane contact interfaces that may fuse slowly, and that the primed state contains macromolecular assemblies of trans-SNARE complexes bound to the Syt1 C<sub>2</sub>B domain and complexin-1 in a spring-loaded configuration that prevents premature membrane merger and formation of extended interfaces but keeps the system ready for fast fusion upon Ca<sup>2+</sup> influx.</p>
All-atom molecular dynamics simulations of synaptic vesicle fusion I: a glimpse at the primed Synaptotagmin-SNARE-complexin complex
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Ketogenic diet dampens excitatory neurotransmission by shrinking synaptic vesicle pools
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Synaptic vesicle glycoprotein 2C enhances vesicular storage of dopamine and counters dopaminergic toxicity
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Data for Adaptor Protein-3 Produces Synaptic Vesicles that Release Phasic Dopamine
<p>Raw data for publication titled Adaptor Protein-3 Produces Synaptic Vesicles that Release Phasic Dopamine.</p>
Data from: Elevated synaptic vesicle release probability in synaptophysin/gyrin family quadruple knockouts
Synaptophysins 1 and 2 and synaptogyrins 1 and 3 constitute a major family of synaptic vesicle membrane proteins. Unlike other widely expressed synaptic vesicle proteins such as vSNAREs and synaptotagmins, the primary function has not been resolved. Here, we report robust elevation in the probability of release of readily releasable vesicles with both high and low release probabilities at a variety of synapse types from knockout mice missing all four family members. Neither the number of readily releasable vesicles, nor the timing of recruitment to the readily releasable pool was affected. The results suggest that family members serve as negative regulators of neurotransmission, acting directly at the level of exocytosis to dampen connection strength selectively when presynaptic action potentials fire at low frequency. The widespread expression suggests that chemical synapses may play a frequency filtering role in biological computation that is more elemental than presently envisioned.
Nicotine-mediated rescue of α-synuclein toxicity requires synaptic vesicle glycoprotein 2
<p>Tabular data underlying all figures. </p>
Data from: Elevated synaptic vesicle release probability in synaptophysin/gyrin family quadruple knockouts
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Ketogenic diet dampens excitatory neurotransmission by shrinking synaptic vesicle pools
GEO Series GSE314901. Mus musculus. 20 samples. Type: Expression profiling by high throughput sequencing.
An iPSC-derived neuronal model of DNAJC6 parkinsonism reveals neurodevelopmental and synaptic vesicle recycling defects
GEO Series GSE208353. Homo sapiens. 15 samples. Type: Expression profiling by high throughput sequencing.
Synaptic vesicle endocytosis deficits underlie GBA-linked cognitive dysfunction in Parkinson’s disease and Dementia with Lewy bodies
GEO Series GSE283187. Mus musculus. 15 samples. Type: Expression profiling by high throughput sequencing.
Ketogenic diet dampens excitatory neurotransmission by shrinking synaptic vesicle pools
GEO Series GSE310481. Mus musculus. 16 samples. Type: Genome binding/occupancy profiling by high throughput sequencing.
Data from: Synaptotagmin 7 functions as a Ca^2+ -sensor for synaptic vesicle replenishment
[No abstract entered]
Data from: Synaptotagmin 7 functions as a Ca^2+ -sensor for synaptic vesicle replenishment
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Allen Brain Atlas
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Annotated Behaviour and Observability Dataset (ABODe)
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