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229 results for “synapse”
Data From: PD-linked LRRK2 G2019S mutation impairs astrocyte morphology and synapse maintenance via ERM hyperphosphorylation
<p>Source data files for Wang et al 'PD-linked LRRK2 G2019S mutation impairs astrocyte morphology and synapse maintenance via ERM hyperphosphorylation'</p>
Local and global predictors of synapse elimination during motor learning
<p>During learning, synaptic connections between excitatory neurons in the brain display considerable dynamism, with new connections being added and old connections eliminated. Synapse elimination offers an opportunity to understand the features of synapses that the brain deems dispensable. However, with limited observations of synaptic activity and plasticity <i>in vivo</i>, the features of synapses subjected to elimination remain poorly understood. Here, we examined the functional basis of synapse elimination in the apical dendrites of L2/3 neurons in the primary motor cortex throughout motor learning. We found no evidence that synapse elimination is facilitated by other local forms of plasticity, or that they reflect less active inputs. Instead, eliminated synapses display asynchronous activity with nearby synapses, suggesting functional synaptic clustering is a critical component of synapse survival. In addition, eliminated synapses show delayed activity timing with respect to postsynaptic output. Thus, synaptic inputs that fail to be co-active with their neighboring synapses or are mistimed with neuronal output are targeted for elimination.</p>
Data for "Synapses without Tension Fail to Fire in an In Vitro Network of Hippocampal Neurons."
<p>Neurons in the brain communicate with each other at their synapses. It has long been understood that this communication occurs through biochemical processes. Here, we reveal a previously unrecognized paradigm wherein mechanical tension in neurons is essential for communication. Using <em>in vitro</em> rat hippocampal neurons, we find that (1) neurons become tout/tensed after forming synapses resulting in a contractile neural network, and (2) without this contractility, neurons fail to fire. To measure time evolution of network contractility in 3D (<em>not</em> 2D) extracellular matrix, we developed an ultra-sensitive force sensor with 1 nN resolution. We employed Multi-Electrode Array (MEA) and iGluSnFR, a glutamate sensor, to quantify neuronal firing at the network and at the single synapse scale, respectively. When neuron contractility is relaxed, both techniques show significantly reduced firing. Firing resumes when contractility is restored. This discovery highlights the essential contribution of neural contractility in fundamental brain functions and has implications for our understanding of neuronal physiology.</p>
Data from: A maximum of two readily releasable vesicles per docking site at a cerebellar single active zone synapse
<p>Recent research suggests that in central mammalian synapses, active zones contain several docking sites acting in parallel. Before release, one or several synaptic vesicles (SVs) are thought to bind to each docking site, forming the readily releasable pool (RRP). Determining the RRP size per docking site has important implications for short-term synaptic plasticity. Here, we take advantage of recently developed methods to count the number of released SVs at single glutamatergic synapses in response to trains of action potentials. In each recording, the number of docking sites was determined by fitting with a binomial model the number of released SVs in response to individual action potentials. After normalization with respect to the number of docking sites, the summed number of released SVs following a train of action potentials was used to estimate of the RRP size per docking site. To improve this estimate, various steps were taken to maximize the release probability of docked SVs, the occupancy of docking sites, as well as the extent of synaptic depression. Under these conditions, the RRP size reached a maximum value close to two SVs per docking site. The results indicate that each docking site contains two distinct SV binding sites that can simultaneously accommodate up to one SV each. They further suggest that under special experimental conditions, as both sites are close to full occupancy, a maximal RRP size of two SVs per docking site can be reached. More generally, the results validate a sequential two-step docking model previously proposed at this preparation.</p>
Synaptopodin regulates denervation-induced plasticity at hippocampal mossy fiber synapses
<p>Neurological diseases can lead to the denervation of brain regions caused by demyelination, traumatic injury or cell death. The molecular and structural mechanisms underlying lesion-induced reorganization of denervated brain regions, however, are a matter of ongoing investigation. In order to address this issue, we performed an entorhinal cortex lesion (ECL) in mouse organotypic entorhino-hippocampal tissue cultures of both sexes and studied denervation-induced plasticity of mossy fiber synapses, which connect dentate granule cells (dGCs) with CA3 pyramidal cells (CA3-PCs) and play important roles in learning and memory formation. Partial denervation caused a strengthening of excitatory neurotransmission in dGCs, CA3-PCs and their direct synaptic connections, as revealed by paired recordings (dGC-to-CA3-PC). These functional changes were accompanied by ultrastructural reorganization of mossy fiber synapses, which regularly contain the plasticity-regulating protein synaptopodin and the spine apparatus organelle. We demonstrate that the spine apparatus organelle and synaptopodin are related to ribosomes in close proximity to synaptic sites and unravel a synaptopodin-related transcriptome. Notably, synaptopodin-deficient tissue preparations that lack the spine apparatus organelle failed to express lesion-induced synaptic adjustments. Hence, synaptopodin and the spine apparatus organelle play a crucial role in regulating lesion-induced synaptic plasticity at hippocampal mossy fiber synapses.</p>
H01 synapse ground truth
<p>Synapse ground truth used for the H01 study.</p> <p>Ground truth used to train a network for synapse identification (see associated paper for details) ares contained in the six Synapse_GT_6_subvolumes.zip</p> <p>Ground truth used for excitatory vs inhibitory classification of identified synapses (see associated paper for details) is contained in the files ei_gt_from_2945_synapses_from_104_proofread_neurons.csv and ei_gt_from_2367_verified_connections.csv</p>
Data from: Clathrin-independent endocytic retrieval of SV proteins mediated by the clathrin adaptor AP-2 at mammalian central synapses
<p><span>Neurotransmission is based on the exocytic fusion of synaptic vesicles (SVs) followed by endocytic membrane retrieval and the reformation of SVs. Conflicting models have been proposed regarding the mechanisms of SV endocytosis, most notably clathrin/ AP-2-mediated endocytosis and clathrin-independent ultrafast endocytosis. Partitioning between these pathways has been suggested to be controlled by temperature and stimulus paradigm. We report on the comprehensive survey of six major SV proteins to show that SV endocytosis in mouse hippocampal neurons at physiological temperature occurs independent of clathrin while the endocytic retrieval of a subset of SV proteins including the vesicular transporters for glutamate and GABA depend on sorting by the clathrin adaptor AP-2. Our findings highlight a clathrin-independent role of the clathrin adaptor AP-2 in the endocytic retrieval of select SV cargos from the presynaptic cell surface and suggest a revised model for the endocytosis of SV membranes at mammalian central synapses.</span></p>
A synaptomic analysis reveals dopamine hub synapses in the mouse striatum : Source Data
<p>Source data for our study on dopamine hub synapses</p> <p>Dopamine transmission is involved in reward processing and motor control, and its impairment plays a central role in numerous neurological disorders. Despite its strong pathophysiological relevance, the molecular and structural organization of the dopaminergic synapse remains to be established. Here, we used targeted labelling and fluorescence activated sorting to purify striatal dopaminergic synaptosomes. We provide the proteome of dopaminergic synapses with 57 proteins specifically enriched. Beyond canonical markers of dopamine neurotransmission such as dopamine biosynthetic enzymes and cognate receptors, we validated 6 proteins not previously described as enriched (Cpne7, Apba1/Mint1, Cadps2, Cadm2/SynCAM 2, Stx4, Mgll). Moreover, our data reveal the adhesion of dopaminergic synapses to glutamatergic, GABAergic or cholinergic synapses in structures we named “dopamine hub synapses”. At glutamatergic synapses, pre- and postsynaptic markers are significantly increased upon association with dopamine synapses. Dopamine hub synapses may thus support local dopaminergic signalling, complementing volume transmission thought to be the major mechanism by which monoamines modulate network activity.</p>
Synapse Competition Data
<p>For the Synpase competition</p>
A B cell actomyosin arc network couples integrin co-stimulation to mechanical force-dependent immune synapse formation
<p>B-cell activation and immune synapse (IS) formation with membrane-bound antigens are actin-dependent processes that scale positively with the strength of antigen-induced signals. Importantly, ligating the B-cell integrin, LFA-1, with ICAM-1 promotes IS formation when antigen is limiting. Whether the actin cytoskeleton plays a specific role in integrin-dependent IS formation is unknown. Here we show using super-resolution imaging of mouse primary B cells that LFA-1: ICAM-1 interactions promote the formation of an actomyosin network that dominates the B-cell IS. This network is created by the formin mDia1, organized into concentric, contractile arcs by myosin 2A, and flows inward at the same rate as B-cell receptor (BCR): antigen clusters. Consistently, individual BCR microclusters are swept inward by individual actomyosin arcs. Under conditions where integrin is required for synapse formation, inhibiting myosin impairs synapse formation, as evidenced by reduced antigen centralization, diminished BCR signaling, and defective signaling protein distribution at the synapse. Together, these results argue that a contractile actomyosin arc network plays a key role in the mechanism by which LFA-1 co-stimulation promotes B-cell activation and IS formation.</p>
Data from: Neurotransmitter content heterogeneity within an interneuron class shapes inhibitory transmission at a central synapse
<p>Neurotransmitter content is deemed the most basic defining criterion for neuronal classes, contrasting with the intercellular heterogeneity of many other molecular and functional features. Here we show, in the adult mouse brain, that neurotransmitter content variegation within a neuronal class is a component of its functional heterogeneity. Most Golgi cells (GoCs), the well-defined class of cerebellar interneurons inhibiting granule cells (GrCs), contain cytosolic glycine, accumulated by the neuronal transporter GlyT2, and GABA in various proportions. To assess the functional consequence of this neurotransmitter variation, we paired GrCs recordings with optogenetic stimulations of single GoCs, which preserve the intracellular transmitter mixture. We show that the strength and decay kinetics of GrCs IPSCs, which are entirely mediated by GABA<sub>A</sub> receptors are negatively correlated to the presynaptic expression of GlyT2 by GoCs. We isolate a slow spillover component of GrCs inhibition that is also affected by the expression of GlyT2, leading to a 56 % decrease in relative charge. Acute manipulations of cytosolic GABA and glycine supply recapitulate the modulation of IPSC charge, supporting the hypothesis that presynaptic loading of glycine negatively impact the GABAergic transmission in mixed interneurons through a competition for vesicular filling. Our results suggest that heterogeneity of neurotransmitter supply within the GoC class may provide a presynaptic mechanism to tune the gain of the stereotypic granular layer microcircuit, thereby expanding the realm of possible dynamic behavior.</p>
Ground truth data used to train the synapse classifier used in Lillvis et al., 2022 for ExLLSM circuit reconstruction
<p class="MsoNormal">Brain function is mediated by the physiological coordination of a vast, intricately connected network of molecular and cellular components. The physiological properties of network components can be quantified with high throughput; the ability to assess many animals per study has been key to relating physiological properties to behavior. Conversely, detailed anatomical properties (e.g., the synaptic connectivity of molecularly-defined cell types across an entire circuit) are presently quantifiable only with low throughput; thus we know very little about how network structure, and structural variation, influences behavior. For neuroanatomical reconstruction there is a methodological gulf between electron-microscopic (EM) methods, which yield dense connectomes (but at great expense and low throughput) and light-microscopic methods, which provide molecular and cell-type specificity with high throughput (but without synaptic resolution). We developed a high-throughput analysis pipeline and imaging protocol using tissue expansion and light sheet microscopy (ExLLSM) to rapidly reconstruct selected circuits across many animals with single-synapse resolution and molecular contrast. Using <em>Drosophila </em>to validate this approach, we demonstrate that it yields synaptic counts similar to those obtained by EM, enables synaptic connectivity to be compared across sex and experience, and can be used to correlate structural connectivity, functional connectivity, and behavior. This approach fills a critical methodological gap in studying variability in the structure and function of neural circuits across individuals within and between species.</p> <p class="MsoNormal">Here, we share the data used to train the synapse classifier that was utilized in the analysis pipeline. All additional software, code, and usage examples to train and run the classifier can be found at Github: <a href="https://github.com/JaneliaSciComp/exllsm-circuit-reconstruction">https://github.com/JaneliaSciComp/exllsm-circuit-reconstruction</a></p>
Synapsed homologs of meiotic mouse chromosomes visualized by TIRFM
<p>Mouse testes were removed from euthanized animals, followed by decapsulation and maceration in high-glucose MEM medium. Suspension was mixed thoroughly and left to settle; the supernatant was then collected and centrifuged at 7200 rpm for 1 min. The pellet was then resuspended in a 0.5 M sucrose solution and added to PFA-treated (1% in 0.015% Triton X-100) coverslides, which were incubated for at room temperature for 2 hours in a humidified environment. After incubation, slides were rinsed twice with a wetting agent solution (Kodak, 1464510) in water and allowed to air dry. SYCP3 was labeled with primary SCP-3 (D-1) antibody (Santa Cruz Biotechnology, SC-74569) and a secondary anti-mouse antibody fused with Alexa-568 (Thermo, A11004). Surface chromosome spreads were imaged in an Elyra 7 microscope (Zeiss), with a 60x 1.4 NA oil immersion objective and an a 1.4x magnification lens. Image reconstruction was performed in ZEN Black with parameters set to default.</p> <p>Experimental procedures were approved by the “Ministero della Salute" of Italy, authorization n.701/2018-PR.</p>
From hidden hearing loss to supranormal auditory processing by neurotrophin 3-mediated modulation of inner hair cell synapse density
<p><span><span>Loss of synapses between spiral ganglion neurons and inner hair cells (IHC synaptopathy), leads to an auditory neuropathy called hidden hearing loss (HHL) characterized by normal auditory thresholds but reduced amplitude of sound-evoked auditory potentials. It has been proposed that synaptopathy and HHL result in poor performance in challenging hearing tasks despite a normal audiogram. However, this has only been tested in animals after exposure to noise or ototoxic drugs, which can cause deficits beyond synaptopathy. Furthermore, the impact of supernumerary synapses on auditory processing has not been evaluated. Here, we studied mice in which IHC synapse counts were increased or decreased by altering neurotrophin 3 (Ntf3) expression in IHC-supporting cells. As we previously showed, postnatal Ntf3 knockdown or overexpression reduces or increases, respectively, IHC synapse density and suprathreshold amplitude of sound-evoked auditory potentials without changing cochlear thresholds. We now show that IHC synapse density does not influence the magnitude of the acoustic startle reflex or its prepulse inhibition. In contrast, gap-prepulse inhibition, a behavioral test for auditory temporal processing, is reduced or enhanced according to Ntf3 expression levels. These results indicate that IHC synaptopathy causes temporal processing deficits predicted in HHL. Furthermore, the improvement in temporal acuity achieved by increasing Ntf3 expression and synapse density suggests a therapeutic strategy for improving hearing in noise for individuals with synaptopathy of various etiologies.</span></span></p>
Activation patterns of afferent synapses on layer 5 tufted pyramidal cells in a biologically detailed simulation
<p>The data set is based on a biologically detailed simulation of a circuit of cortical neurons. The circuit was activated by thalamo-cortical inputs every 1 s for 500 ms. We report for a number of exemplary tufted pyramidal cells in layer 5 the pattern activation of their afferent synapses.</p> <p>Specifically, we report for all afferent excitatory synapses the pairwise path distances along the dendrite / soma (note that the soma was simplified to a point for the purpose of calculating path distances, but not during the simulation), and the times of activation of each of these synapses.</p> <p>The simulation is based on the model described in <a href="https://www.biorxiv.org/content/10.1101/2022.08.11.503144v1">this preprint</a>. The model can also be found <a href="https://zenodo.org/record/6906785">here on Zenodo</a>. For more details on the simulation, contact the author.</p> <p>For more details about the format of the data, refer to the included jupyter notebook.</p>
Large-scale survey of excitatory synapses reveals sublamina-specific and asymmetric synapse disassembly patterns in a neurodegenerative circuit
<p>Dataset associated with the manuscript titled "<strong>Large-scale survey of excitatory synapses reveals sublamina-specific and asymmetric synapse disassembly patterns in a neurodegenerative circuit"</strong></p>
The amyloid precursor protein regulates synaptic transmission at medial perforant path synapses
<p><span>The perforant path provides the primary cortical excitatory input to the hippocampus. Due to its important role in information processing and coding, entorhinal projections to the dentate gyrus have been studied in considerable detail. Nevertheless, synaptic transmission between individual connected pairs of entorhinal </span><span>stellate cells and dentate granule cells</span><span> remains to be characterized. Here, we have used mouse organotypic entorhino-hippocampal tissue cultures of either sex, in which the entorhino-dentate (EC-GC) projection is present and EC-GC pairs can be studied using whole-cell patch clamp recordings. By using cultures of wildtype mice, the properties of EC-GC synapses formed by afferents from the lateral and medial entorhinal cortex were compared and differences in short-term plasticity were identified. Since the perforant path is severely affected in Alzheimer´s disease, we used tissue cultures of amyloid-precursor protein (APP)-deficient mice to examine the role of APP at this synapse. APP deficiency altered excitatory neurotransmission at medial perforant path synapses, which was accompanied by transcriptomic and ultrastructural changes. Moreover, presynaptic but not postsynaptic APP deletion through the local injection of Cre-expressing adeno-associated viruses in conditional APP<sup>flox/flox</sup> tissue cultures increased the neurotransmission efficacy at perforant path synapses. In summary, these data suggest a physiological role for presynaptic APP at medial perforant path synapses that may be adversely affected under altered APP processing conditions.</span></p>
Differential Short-Term Facilitation Of Synaptic Inputs And Spike Transmission At The Retinocollicular Synapse In Vivo
<p>Neuropixels data for investigating short-term plasticity in the mouse retinocollicular pathway. </p> <p>Paper (bioRxiv): <a href="https://www.biorxiv.org/content/10.1101/2024.01.17.576068v1">Differential Short-Term Facilitation Of Synaptic Inputs And Spike Transmission At The Retinocollicular Synapse In Vivo</a></p> <p>Full data will be availale upon publication of the paper.</p>
SYN120 Study to Evaluate Its Safety, Tolerability and Efficacy in Parkinson's Disease Dementia (SYNAPSE)
ClinicalTrials.gov study NCT02258152. IPD Sharing: Not stated. Countries: 1. Publications: 1.
Data from: Neurotransmitter content heterogeneity within an interneuron class shapes inhibitory transmission at a central synapse
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