Find research datasets worth reusing
Search datasets from major research repositories and use ShareScore to quickly assess how well each record supports discovery, access, and reuse.
97
datasets available to search
ShareScore release 0.9.0
Dataset results
97 results for “Synaptic plasticity”
Raw data for: "CalDAG-GEFI mediates striatal cholinergic modulation of dendritic excitability, synaptic plasticity and psychomotor behaviors"
<p>Figure 2. CDGI mediates the M1R modulation of dendritic excitability but not the M1R</p> <p>modulation of somatic excitability.</p> <p>(A and B) Sagittal sections through the brains of CDGI knockout mice in which the direct</p> <p>pathway was visualized (red) in D1-tdTomato mice (A) and the indirect pathway was visualized</p> <p>(green) in D2-GFP mice.</p> <p>(C) Sample somatic voltage changes evoked by 120pA current injections in iSPNs from WT</p> <p>(black) and CDGI-KO (red) before and after bath application of oxo-M (10 µM).</p> <p>(C-D) Current-response curves of iSPNs from WT (B, n=5 cells) and CDGI-KO mice (C, n=7</p> <p>cells). Somatic excitability of iSPNs was similarly enhanced by oxo-M in WT and CDGI-KO.</p> <p>(E) Sample somatic recordings in response to 140pA current injections in dSPNs from WT</p> <p>(black) and CDGI KO (red) before and after bath application of oxo-M (10 µM).</p> <p>(F-H) Current-response curves of dSPNs from WT (E) and CDGI-KO (F) mice (n=4-6).</p> <p>(I) Trains of five EPSPs were evoked by stimulation of glutamatergic afferent fibers at 40 Hz.</p> <p>Oxo-M (10 µM) increased EPSP summation in iSPNs of WT, but not in CDGI-KO or when</p> <p>M1Rs were blocked by M1R antagonist VU0255035 in WT (5 M).</p> <p>(J) Box plot showing the effect of oxoM on synaptic summation. The EPSP5/EPSP1 ratio was</p> <p>increased by oxoM in iSPNs of WT (p = 0.002, Wilcoxon test; n = 10), but not in iSPNs of 27</p> <p>CDGI-KO mice (p = 0.25, n = 9) or in iSPNs of WT mice in the presence of VU0255035 (p =</p> <p>0.69, n = 6).</p> <p>(K) Box plot showing the effect of oxoM on the kinetics of synaptic response. The decay time</p> <p>constant of EPSP5 was significantly increased by oxoM in iSPNs of WT (p = 0.002); but not</p> <p>when CDGI was genetically deleted (p = 0.65) or when M1R was pharmacologically blocked (p</p> <p>= 0.84).</p>
Raw data for Facemasks and face recognition: Potential impact on synaptic plasticity
<p>Figure 2 legend Upper panel. In control condition, visual sensory inputs from in- dividual’s face are encoded by the face recognition system. At system level (a), this process implies functional and structural modifications in multiple brain regions, whereas at cellular level (b), this promotes the induction of distinct forms of synaptic plasticity, such as long-term potentiation and long-term depression (LTP, LTD, respectively). Lower panel. Wearing face masks consis- tently reduces the amount of information, by excluding the lower part of the face, including nose and mouth. Thus, both at system and cellular level, such mismatch impairs long-term functional and structural plasticity. In particular, at synaptic level, LTP induction will be favored, whereas LTD will be impaired. The black traces indicate the excitatory postsynaptic potentials in control condition; the red traces represent the long-term changes in synaptic efficacy after the induction protocol.</p>
Raw data for: "Vesicular Acetylcholine Transporter Alters Cholinergic Tone and Synaptic Plasticity in DYT1 Dystonia"
<p>Raw data for Supplemental Figure 2 - Patch-Clamp recordings of ChI firing activity after bath application of donepezil (Donep 50 μM, 5 minutes). The inhibition by donepezil was weaker in Tor1a+/− than in Tor1a+/+ neurons.</p>
A sequential two-step priming scheme reproduces diversity in synaptic strength and short-term plasticity
<p>Please consult the uploaded word file '<a href="https://zenodo.org/api/files/274d8784-bd00-47da-b7e7-7350c0aa3659/figure_4_public.docx">figure_4_public.docx</a>' for a description.</p>
Adiponectin rescues synaptic plasticity in the dentate gyrus of a mouse model of fragile X syndrome
<p>Fragile X Syndrome (FXS) is the most common inherited cause of intellectual disability and is the leading known single-gene cause of autism spectrum disorder. FXS patients display varied behavioural deficits that include mild to severe cognitive impairments in addition to mood disorders. Currently, there is no cure for this condition, however, there is an emerging focus on therapies that inhibit mTOR-dependent protein synthesis due to the clinical effectiveness of metformin for alleviating some behavioural symptoms in FXS. Adiponectin (APN) is a neurohormone that is released by adipocytes and provides an alternative means to inhibit mTOR activation in the brain. In these studies, we show that <em>Fmr1</em> KO mice, like FXS patients, show reduced levels of circulating APN, and that both LTP and LTD in the DG (dentate gyrus) are impaired. Brief (20 min) incubation of hippocampal slices in APN (50 nM) was able to rescue both LTP and LTD in the DG and increased both the surface expression and phosphorylation of GluA1 receptors. These results provide evidence for reduced adiponectin levels in FXS playing a role in decreasing bidirectional synaptic plasticity and show that therapies that enhance adiponectin levels may have therapeutic potential for this and related conditions.</p>
Stochastic synaptic plasticity underlying compulsion in an addiction model
<p>Data set for article published in Nature: Pascoli 2018 https://doi.org/10.1038/s41586-018-0789-4</p>
Dataset from Maith, O., Baladron, J., Einhäuser, W., & Hamker, F. H. (2023). Exploration behavior after reversals is predicted by STN-GPe synaptic plasticity in a basal ganglia model. Submitted to iScience.
<p>This dataset contains all analyzed data from the study "Maith, O., Baladron, J., Einhäuser, W., & Hamker, F. H. (2023). Exploration behavior after reversals is predicted by STN-GPe synaptic plasticity in a basal ganglia model. Submitted to iScience.". It includes the behavioral data of 20 human participants (folder "psychExp") and of simulations of a neuro-computational basal ganglia model (folder "simulations") of the study.</p> <p>To replicate the results of the study, the dataset can be analyzed using the code provided separately under the following identifier: https://doi.org/10.5281/zenodo.6555886. The dataset is organized in the directory structure required for this purpose.</p> <p>For the human participants, only preprocessed eye-tracking and general behavioral data (.mat files) and the final analyzed behavioral data (output files) generated with the script "get_vps_outputs.m" (folder psychExp/..../3_srcAna/) are available. For more information about preprocessing steps as well as raw data of the eye-tracking experiment, please contact us by email (click <a href="https://www.tu-chemnitz.de/urz/mail/adrx.html?1-d29sZmdhbmcuZWluaGFldXNlci10cmV5ZXJAcGh5c2lrLg==">here</a>).</p>
Denervated mouse CA1 pyramidal neurons express homeostatic synaptic plasticity following entorhinal cortex lesion
<p><span>Structural, functional, and molecular reorganization of denervated neural networks is often observed in neurological conditions. The loss of input is accompanied by homeostatic synaptic adaptations, which can affect the reorganization process. A major challenge of denervation-induced homeostatic plasticity operating in complex neural networks is the specialization of neuronal inputs. It remains unclear whether neurons respond similarly to the loss of distinct inputs. Here, we used <em>in</em> <em>vitro</em> entorhinal cortex lesion (ECL) and Schaffer collateral lesion (SCL) in mouse organotypic entorhino-hippocampal tissue cultures to study denervation-induced plasticity of CA1 pyramidal neurons. We observed microglia accumulation, presynaptic bouton degeneration, and a reduction in dendritic spine numbers in the denervated layers three days after SCL and ECL. Transcriptome analysis of the CA1 region revealed complex changes in differential gene expression following SCL and ECL compared to non-lesioned controls with a specific enrichment of differentially expressed synapse-related genes observed after ECL. Consistent with this finding, denervation-induced homeostatic plasticity of excitatory synapses was observed three days after ECL but not after SCL. Chemogenetic silencing of the EC but not CA3 confirmed the pathway-specific induction of homeostatic synaptic plasticity in CA1. Additionally, increased RNA oxidation was observed after SCL and ECL. These results reveal important commonalities and differences between distinct pathway lesions and demonstrate a pathway-specific induction of denervation-induced homeostatic synaptic plasticity. </span></p>
Microglia modulate TNFα‐mediated synaptic plasticity
<p>The pro-inflammatory cytokine tumor necrosis factor α (TNFα) tunes the capacity of neurons to express synaptic plasticity. It remains, however, unclear how TNFα mediates synaptic positive (=change) and negative (=stability) feedback mechanisms. We assessed effects of TNFα on microglia activation and synaptic transmission onto CA1 pyramidal neurons of mouse organotypic entorhino–hippocampal tissue cultures. TNFα mediated changes in excitatory and inhibitory neurotransmission in a concentration-dependent manner, where low concentration strengthened glutamatergic neurotransmission via synaptic accumulation of GluA1-only-containing AMPA receptors and higher concentration increased inhibition. The latter induced the synaptic accumulation of GluA1-only-containing AMPA receptors as well. However, activated, pro-inflammatory microglia mediated a homeostatic adjustment of excitatory synapses, that is, an initial increase in excitatory synaptic strength at 3 h returned to baseline within 24 h, while inhibitory neurotransmission increased. In microglia-depleted tissue cultures, synaptic strengthening triggered by high levels of TNFα persisted and the impact of TNFα on inhibitory neurotransmission was still observed and dependent on its concentration. These findings underscore the essential role of microglia in TNFα-mediated synaptic plasticity. They suggest that pro-inflammatory microglia mediate synaptic homeostasis, that is, negative feedback mechanisms, which may affect the ability of neurons to express further plasticity, thereby emphasizing the importance of microglia as gatekeepers of synaptic change and stability.</p>
Microglia modulate TNFα‐mediated synaptic plasticity
Open the record for dataset details and reuse information.
All-trans retinoic acid induces synaptic plasticity in human cortical neurons
Open the record for dataset details and reuse information.
Adiponectin rescues synaptic plasticity in the dentate gyrus of a mouse model of fragile X syndrome
Open the record for dataset details and reuse information.
Denervated mouse CA1 pyramidal neurons express homeostatic synaptic plasticity following entorhinal cortex lesion
Open the record for dataset details and reuse information.
Intrinsic and synaptic determinants of receptive field plasticity in Purkinje cells of the mouse cerebellum
<p>Here we provide the data for the paper "Intrinsic and synaptic determinants of receptive field plasticity in Purkinje cells of the mouse cerebellum". The dataset is saved as MAT-file (version 7.0). The source code for analysis is saved in github. Folder names indicate the contents corresponding to the specific figures in the paper.</p>
Synaptic plasticity model datasets
<p>These datasets are used to reproduce the results of the synaptic plasticity model from the paper https://doi.org/10.1101/725382.</p>
High-resolution imaging and manipulation of endogenous AMPA receptor surface mobility during synaptic plasticity and learning
<p><span>Data set for the MS</span></p>
Visualizing synaptic plasticity in vivo by large-scale imaging of endogenous AMPA receptors
<p>Elucidating how synaptic molecules such as AMPA receptors mediate neuronal communication and tracking their dynamic expression during behavior is crucial to understand cognition and disease, but current technological barriers preclude large-scale exploration of molecular dynamics in vivo. We have developed a suite of innovative methodologies that break through these barriers: a new knockin mouse line with fluorescently tagged endogenous AMPA receptors, two-photon imaging of hundreds of thousands of labeled synapses in behaving mice, and computer vision-based automatic synapse detection. Using these tools, we can longitudinally track how the strength of populations of synapses changes during behavior. We used this approach to generate an unprecedentedly detailed spatiotemporal map of synapses undergoing changes in strength following sensory experience. More generally, these tools can be used as an optical probe capable of measuring functional synapse strength across entire brain areas during any behavioral paradigm, describing complex system-wide changes with molecular precision.</p>
Dataset for "A critical role for CaMKII in behavioral timescale synaptic plasticity in hippocampal CA1 pyramidal neurons"
<p>Dataset for "A critical role for CaMKII in behavioral timescale synaptic plasticity in hippocampal CA1 pyramidal neurons"</p>
Synaptic Plasticity and Cognitive Function in RASopathies
ClinicalTrials.gov study NCT03504501. IPD Sharing: NO. Countries: 1. Publications: 2.
Enhancing Synaptic Plasticity and Cognition in Schizophrenia
ClinicalTrials.gov study NCT01776112. IPD Sharing: Not stated. Countries: 1. Publications: 1.
ScienceDex guides
Understand access before you commit
These curated guides explain access requirements, typical timelines, costs, and reuse considerations for widely used research datasets.
Allen Brain Atlas
Allen Brain Atlas is an Allen Institute collection of brain map atlases, datasets, APIs, and analysis tools covering mouse, human, and non-human primate brain resources.
Annotated Behaviour and Observability Dataset (ABODe)
ABODe is a University of Edinburgh DataShare dataset for behavior classification in group-housed mice using home-cage video, identities, bounding boxes, ground-plate positions, and annotator labels.
DANDI Archive for NWB datasets
DANDI is a BRAIN Initiative archive for publishing and sharing neurophysiology data, including electrophysiology, optophysiology, and behavioral data packaged as NWB and related standards.
International Brain Laboratory public data
The International Brain Laboratory public data releases expose standardized mouse decision-making experiments, including Neuropixels recordings, widefield calcium imaging, behavior, and session metadata accessed through the ONE API.
OpenNeuro
OpenNeuro is a free, open platform for sharing neuroimaging datasets, with public search, dataset pages, and download paths for web, S3, DataLad, and the OpenNeuro CLI.