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520 results for “Dopamine”
Overlapping representations of food and social stimuli in VTA dopamine neurons
<p>2-photon imaging and behavioral data accompanying publication of "Overlapping representations of food and social stimuli in VTA dopamine neurons" (Lindsay Willmore, Adelaide Minerva, Ben Engelhard, Brenna McMannon, Nirja Oak, Stephan Thiberge, Malavika Murugan, Catherine Jensen Pena, Ilana Witten). This dataset contains all information required to recreate figures from the paper. </p>
Genetic Effects on Dopamine Response to an Opiate
ClinicalTrials.gov study NCT01878006. IPD Sharing: UNDECIDED. Countries: 1. Publications: 4.
Evolution of a central dopamine circuit underlies adaptation of light-evoked sensorimotor response in the blind cavefish, <em>Astyanax mexicanus</em>
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Data for: Natural genetic variation in a dopamine receptor is associated with variation in female fertility in Drosophila melanogaster
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Overlapping representations of food and social stimuli in VTA dopamine neurons
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Data from: A proprioceptive feedback circuit drives C. elegans locomotor adaptation through dopamine signaling
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Mesolimbic dopamine neurons drive infradian rhythms in sleep-wake and heightened activity state
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Dopamine mediates the pea aphid wing plasticity
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Data from: Oxytocin and dopamine receptor expression: Cellular level implications for pair bonding
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Data from: Whole-organism behavioral profiling reveals a role for dopamine in state-dependent motor program coupling in C. elegans.
<p>Animal behaviors are commonly organized into long-lasting states that coordinately impact the generation of diverse motor outputs such as feeding, locomotion, and grooming. However, the neural mechanisms that coordinate these diverse motor programs remain poorly understood. Here, we examine how the distinct motor programs of the nematode <i>C. elegans </i>are coupled together across behavioral states. We describe a new imaging platform that permits automated, simultaneous quantification of each of the main <i>C. elegans</i> motor programs over hours or days. Analysis of these whole-organism behavioral profiles shows that the motor programs coordinately change as animals switch behavioral states. Utilizing genetics, optogenetics, and calcium imaging, we identify a new role for dopamine in coupling locomotion and egg-laying together across states. These results provide new insights into how the diverse motor programs throughout an organism are coordinated and suggest that neuromodulators like dopamine can couple motor circuits together in a state-dependent manner. </p>
Data for Chronic hyperactivation of midbrain dopamine neurons causes preferential dopamine neuron degeneration
<p>Raw Data for publication titled Chronic hyperactivation of midbrain dopamine neurons causes preferential dopamine neuron degeneration.</p>
Data from: Acetylcholine waves and dopamine release in the striatum
<p>Striatal dopamine encodes reward, with recent work showing that dopamine release occurs in spatiotemporal waves. However, the mechanism of dopamine waves is unknown. Here we report that acetylcholine release in mouse striatum also exhibits wave activity, and that the spatial scale of striatal dopamine release is extended by nicotinic acetylcholine receptors. Based on these findings, and on our demonstration that single cholinergic interneurons can induce dopamine release, we hypothesized that the local reciprocal interaction between cholinergic interneurons and dopamine axons suffices to drive endogenous traveling waves. We show that the morphological and physiological properties of cholinergic interneuron – dopamine axon interactions can be modeled as a reaction-diffusion system that gives rise to traveling waves. Analytically-tractable versions of the model show that the structure and the nature of propagation of acetylcholine and dopamine traveling waves depend on their coupling, and that traveling waves can give rise to empirically observed correlations between these signals. Thus, our study provides evidence for striatal acetylcholine waves <em>in vivo</em>, and proposes a testable theoretical framework that predicts that the observed dopamine and acetylcholine waves are strongly coupled phenomena.</p>
Interspecies chimerism with human embryonic stem cells generates functional human dopamine neurons at low efficiency
<p>Interspecies chimeras offer great potential for regenerative medicine and creation of human disease models. Whether human pluripotent stem cell (hPSC) derived neurons in an interspecies chimera can differentiate into functional neurons and integrate into host neural circuity is not known. Here we show, using Engrailed 1 (En1) as a development niche that human naïve-like ES cells can incorporate into embryonic and adult mouse brains. Human-derived neurons including tyrosine hydroxylase (TH) positive neurons integrate into the mouse brain at low efficiency. These TH-positive neurons have electrophysiologic properties consistent with their human origin. Additionally, these human-derived neurons in the mouse brain accumulate pathologic phosphorylated α-synuclein in response to α-synuclein preformed fibrils. Optimization of human/mouse chimeras could be utilized to study human neuronal differentiation and human brain disorders.</p>
Recovery from social isolation requires dopamine in males, but not the autism-related gene nlg3 in either sex
<p>Social isolation causes profound changes in social behaviour in a variety of species. However, the genetic and molecular mechanisms modulating behavioural responses to social isolation and social recovery remain to be elucidated. Here, we quantified the behavioural response of vinegar flies to social isolation using two distinct protocols (social space preference and spontaneous tendencies to form groups). We found that social isolation increased social space and reduced sociability. These effects of social isolation were reversible and could be reduced after 3 days of group housing. Flies with a loss of function of <em>neuroligin3</em> (ortholog of autism-related <em>neuroligin</em> genes) with known increased social space in a socially enriched environment, were still able to recover from social isolation. We also show that dopamine is needed for a response to social isolation and recovery in males but not in females. Furthermore, only in males, dopamine levels are reduced after isolation and are not recovered after group housing. Finally, in socially enriched flies mutant for <em>neuroligin3</em>, dopamine levels are reduced in males, but not in females. We propose a model to explain how dopamine and <em>neuroligin3</em> are involved in the behavioural response to social isolation and its recovery in a dynamic and sex-specific manner.</p>
Dataset associated with the study entitled "Dopamine lesions alter the striatal encoding of single-limb gait"
<p>There are two compressed <strong>dataset </strong>files. </p> <p>The file <strong>data.zip</strong> contains a dataset consisting of electrophysiological and behavioral measurements in the dorsal striatum of mice freely behaving in a 60 cm x 60 cm open field. Optogenetic tagging was performed to identify D1 or D2 MSNs.</p> <p>There are three experimental groups in the file <strong>data.zip</strong>:</p> <p>1. HL....the healthy group</p> <p>2. PD....the dopamine lesioned group (unilateral 6OHDA injection in the medial forebrain bundle)</p> <p>3. CT....the sham lesioned control group</p> <p>There is one experimental group in the file <strong>D2_stim_gait.zip</strong>:</p> <p>1. Behavioral measurements during optogenetic stimulation of D2 MSNs to assess changes in gait performance.</p> <p><strong>Code </strong>for analyzing the data is available at: https://github.com/LongYang10/Gait-Analysis-of-Freely-Walking-Mouse</p>
Data from: Comparison of dopamine release and uptake parameters across sex, species and striatal subregions
<p><span>Dopamine in the striatum strongly regulates behavioral output in a heterogenous across the various striatal subregions. Moreover, dopamine dynamics not only displays heterogeneity across brain structures but also within males and females. The purpose of this dataset was to evaluate the dopamine dynamics in male and female mice and rats across five subregions: the dorsolateral caudate, ventromedial caudate, nucleus accumbens core, nucleus accumbens lateral shell, and the nucleus accumbens medial shell. Fast scan cyclic voltammetry (FSCV) was employed to measure dopamine release and uptake following a single pulse electrical stimulation in each of these subregions within a single brain slice. The dopamine dynamics were also observed across a variety of stimulation amplitudes. The goal of this dataset was to produce systematic FSCV measurements of dopamine across the rodent striatum using FSCV which would be available as a </span><span>resource for further investigation of DA terminal function.</span></p>
Data from: Neuronal function and dopamine signaling evolve at high temperature in Drosophila
<p>Neuronal activity is temperature sensitive and affects behavioral traits important for individual fitness, such as locomotion and courtship. Yet, we do not know enough about the evolutionary response of neuronal phenotypes in new temperature environments. Here, we use long-term experimental evolution of <em>Drosophila simulans</em> populations exposed to novel temperature regimes. Here, we demonstrate a direct relationship between thermal selective pressure and the evolution of neuronally expressed molecular and behavioral phenotypes. Several essential neuronal genes evolve lower expression at high temperatures and higher expression at low temperatures, with dopaminergic neurons standing out by displaying the most consistent expression change across independent replicates. We functionally validate the link between evolved gene expression and behavioral changes by pharmacological intervention in the experimentally evolved <em>D. simulans</em> populations as well as by genetically triggered expression changes of key genes in <em>D. melanogaster</em>. As natural temperature clines confirm our results for <em>Drosophila</em> and <em>Anopheles</em>populations, we conclude that neuronal dopamine evolution is a key factor for temperature adaptation.</p>
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>
Rapid modulation of striatal cholinergic interneurons and dopamine release by satellite astrocytes
<h3><strong>ABSTRACT</strong></h3> <p>Astrocytes are increasingly thought to possess underestimated and important roles in modulating neuronal circuits. Astrocytes in striatum can regulate dopamine transmission by governing the extracellular tone of axonal neuromodulators, including GABA and adenosine. However, here we reveal that striatal astrocytes occupy a cell type-specific anatomical and functional relationship with cholinergic interneurons (ChIs), through which they rapidly excite ChIs and govern dopamine release via nicotinic acetylcholine receptors on subsecond timescales. We identify that ChI somata are in unexpectedly close proximity to astrocyte somata, in mouse and human, forming a “soma-to-soma” satellite-like configuration not typically observed for other striatal neurons. Transient depolarization of astrocytes in mouse striatum reversibly regulated ChI excitability by decreasing extracellular calcium. These findings reveal a privileged satellite astrocyte-interneuron interaction for striatal ChIs operating on subsecond timescales via regulation of extracellular calcium dynamics to shape downstream striatal circuit activity and dopamine signaling.</p> <p> </p> <h3><strong>FILE DESCRIPTIONS</strong></h3> <p>This repository contains the following files:</p> <ul> <li>Key Resources Table (.xlsx) - Table containing details on key resources (antibodies, mouse lines, virus strains, software, equipment, and reagents), and the persistent identifiers for protocols and code used and generated in this study. </li> <li>Source Data Folder (.zip): <ul> <li>_README_Source_Data (.txt) with detailed information about each dataset.</li> <li>Individual tabular datasets corresponding to each panel shown in the Main Figures 1 to 5 (.csv).</li> <li>Excel spreadsheet containing all tabular datasets plotted in Main Figures 1 to 5 (.xlsx)</li> </ul> </li> <li>Supplementary Data Folder (.zip): <ul> <li>_README_Supplementary_Data (.txt) with detailed information about each dataset.</li> <li>Individual tabular datasets corresponding to each panel shown in the Supplementary Figures 1-9, 11-14 (.csv).</li> <li>Excel spreadsheet containing all tabular datasets plotted in Supplementary Figures 1-9, 11-14 (.xlsx)</li> </ul> </li> </ul>
An axonal brake on striatal dopamine output by cholinergic interneurons
<h3><strong>ABSTRACT</strong></h3> <p>Depolarisation of distal axons is necessary for somatic action potentials to be translated into axonal neurotransmitter release. Here, we show that activation of striatal cholinergic interneurons (ChIs) and nicotinic receptors (nAChRs) on mouse DA axons transiently prevents the release of dopamine (DA) by subsequent stimuli for ~100 ms. Previous studies have shown that nAChRs on DA axons can drive ectopic action potentials in DA axons to trigger DA release. We demonstrate <em>ex vivo </em>that a lower level of activation of ChIs is needed to suppress DA release than to trigger it, an effect that is not due to DA depletion, but to restricted re-activation of DA axons. This axonal brake on DA output is stronger and more persistent in dorsal than ventral striatum. <em>In vivo</em>, we reveal a predominant depression of DA release by endogenous acetylcholine, as antagonism of nAChRs in dorsal striatum conversely elevated tonic DA detected with optic-fibre photometry of GRAB<sub>DA2m</sub> sensor and promoted conditioned place-preference. Our findings reveal that ChIs acting via nAChRs limit activation of DA axons by subsequent DA neuron activity, uncoupling DA axons from ascending action potentials and generating a dynamic inverse scaling of DA release according to ChI activity.</p> <p> </p> <h3><strong>FILE DESCRIPTIONS</strong></h3> <p>This repository contains the following files:</p> <ul> <li>Key Resources Table (.xlsx) - Table containing details on key resources (antibodies, mouse lines, virus strains, and software), and the persistent identifiers for protocols and code used and generated in this study. </li> <li>Source Data Folder (.zip): <ul> <li>_README_Source_Data (.txt) with detailed information about each dataset.</li> <li>Individual tabular datasets corresponding to panels shown in the Main Figures 1 to 5 (.csv).</li> <li>Excel spreadsheet containing all tabular datasets plotted in Main Figures 1 to 5 (.xlsx)</li> </ul> </li> <li>Supplementary Data Folder (.zip): <ul> <li>_README_Supplementary_Data (.txt) with detailed information about each dataset.</li> <li>Individual tabular datasets corresponding to panels shown in the Supplementary Figures 1 to 6 (.csv).</li> <li>Excel spreadsheet containing all tabular datasets plotted in Supplementary Figures 1 to 6 (.xlsx)</li> </ul> </li> </ul>
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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.
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DANDI Archive for NWB datasets
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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.