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1,211 results for “Gestation”
Gestational Cd exposure in the CD-1 mouse induces sex-specific hepatic insulin insensitivity, obesity and metabolic syndrome in adult female offspring
<p>There is compelling evidence that developmental exposure to some toxic metals increases risk for obesity and obesity-related morbidity including cardiovascular disease and type 2 diabetes in adults. To explore the hypothesis that developmental Cd exposure increased risk of obesity later in life, male and female CD-1 mice were maternally exposed to 500 ppb CdCl<sub>2</sub> in drinking water during a human gestational equivalent period (GD0 - PND10). Hallmark indicators of metabolic disruption, hepatic steatosis, and metabolic syndrome were evaluated prior to birth through adulthood. Blood Cd levels in dams were similar to those observed in human pregnancy cohorts. There were no observed impacts of exposure on dams or pregnancy-related outcomes. Results of glucose and insulin tolerance testing revealed that Cd-exposure impaired glucose homeostasis in young adult offspring. Exposure-related increases in circulating triglycerides and hepatic steatosis were apparent only in females. By PND120, Cd-exposed females had become 30% heavier with 700% more perigonadal fat than unexposed control females. There was no evidence of dyslipidemia, steatosis, increased weight gain, nor increased adiposity in Cd-exposed male offspring. Hepatic transcriptome analysis at PND1, PND21, and PND42 revealed evidence for female-specific increases in oxidative stress and mitochondrial dysfunction with significant early disruption of retinoic acid signaling and altered insulin receptor signaling consistent with hepatic insulin sensitivity in adult females. The observed steatosis and metabolic syndrome-like phenotypes resulting from exposure to 500 ppb CdCl<sub>2</sub> during the pre- and perinatal period of development equivalent to human gestation indicate that Cd acts developmentally as a sex-specific delayed obesogen.</p>
Longitudinal structural MRI, MRS, and behavioral data for mice prenatally exposed to maternal immune activation at gestational day 9
<p>Previous evidence from our lab (https://cobralab.ca/) and others suggest that prenatal exposure to maternal immune activation (MIA) can impact trajectories of neurodevelopment as measured through brain anatomy and behavior in mice. Yet, there are still open questions regarding the alterations to developmental trajectories, as well as the impact on brain chemistry, that this data set seeks to explore. The dataset presented here includes magnetic resonance imaging (MRI) and magnetic resonance spectroscopy (MRS) data from two timepoints, adolescence (postnatal day [PND 35]) and young adulthood (PND 60) in C57BL/6J mice prenatally exposed either to poly I:C (POL) inducing maternal immune activation (MIA) or saline (SAL) at gestational day (GD) 9. The dataset also includes three behaviors acquired after each scanning session with 2 days of rest between the scans and each behavior: open field test, social novel object preference test, and prepule inhibition. Finally, the data also include cytokine assays acquired from a separate sample of pregnant mice and a test-retest of MRS acquired from a voxel in the anterior cingulate area. </p> <p>The data here published were collected and analyzed for a paper under review, available as a preprint where more details can be found here: https://www.preprints.org/manuscript/202203.0136/v1. In brief, using whole-brain, voxelwise analysis techniques (deformation-based morphometry) we found MIA subtly altered developmental trajectories, reducing volume relative to SAL offspring in the hippocampus and the anterior, right caudate putamen, and increasing volume in the posterior, left caudate putamen and cerebellum. Additionally, there was a trending decrease of myo-inositol and GABA in MIA offspring at PND 60 compared to SAL controls. Finally, there was a trending decrease in ratio of distance travelled in the anxiogenic center zone of an open field compared to the outer areas at PND 35 for MIA offspring. </p> <p>In this dataset you will find a total of <strong>80 preprocessed structural MRIs</strong> in minc format acquired at postnatal day ~35 and ~60 in mice exposed to 5mg/kg poly I:C or vehicle control (0.9% sterile saline) at GD9. The images are included in CUPO_MIA_mncs.zip. These are T1-weighted structural images with two averages; repetition time (TR)/echo time (TE) = 21.55 ms/5.13 ms, matrix size = 260 x 158 x 210, voxel dimensions =&thinsp;70 µm isotropic, flip angle =&thinsp;20°, 23 min total using 5% isoflurane for induction, 1.5% for maintenance of anesthesia during the scan on a cryogenically-cooled surface coil. T1-weighted scans were preprocessed by stripping native coordinates, flipping left-right to maintain fidelity, denoising, correcting inhomogeneities in the bias field using the N4 algorithm, and registering in LSQ6 alignment (i.e. 6 degrees of freedom are allowed for imagine alignment: translations and rotations along x, y, and z dimensions). The demographics information for each animal is included in the <strong>demographics.csv</strong> file. </p> <p>Behavioural tests were performed following the postnatal day 35 and 60 scans in all animals with a 2 day rest period. These include: open field test, three chambered social approach, and prepulse inhibition. The data for all of these tests is presented in individual .csv spreadsheet and includes data for both the timepoints evaluated. Additionally, cytokine panels were collected from an independent cohort of 7 dams. <strong>MRS </strong>data are included in two formats: 1) preprocessed quantifications from LCModel software in csvs, and 2) raw data with press and press_w (respectively water supressed and unsupressed acquisitions) for analysis. The raw data were released in upload version 1.1.0. MRS was acquired from a 1.2 x 2.6 x 2.5 mm3 voxel in the ACA with a Point Resolved Spectroscopy sequence (PRESS; TR/TE=3000/8.5 ms, 256 averages). Within the raw_data.zip,</p> <p>Included in this data set are the structural MRIs in MINC format, the behavioural .csv data, the MRS data (csvs and raw files), and a <strong>README</strong> file providing further detail on the data structure and content, and on how to interpret the data column titles. DICOMS are also available for the structural MRI data, as are the raw (not-preprocessed) MINC files, available upon request to the authors. </p>
Vitamin B12 deficiency anaemia and gestational diabetes mellitus: a two-sample Mendelian randomization study
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Longitudinal structural MRI and behavioural data for mice prenatally exposed to maternal immune activation either early or late in gestation
<p>Prenatal maternal immune activation (MIA) is a risk factor for neurodevelopmental disorders. How the gestational timing of MIA-exposure differentially impacts downstream development remains unclear. The data presented here includes longitudinal structural magnetic resonance imaging (MRI) data from weaning to adulthood, and behavioural testing in adolescence and adulthood on C57BL/6 mice exposed to MIA induced by the viral mimetic, polyinosinic:polycytidylic acid (poly I:C) either early (gestational day [GD]9) or late (GD17) in gestation. </p> <p>The data published here was collected and analyzed for the following publication, where more details can be found (Guma et al., 2021 https://doi.org/10.1016/j.biopsych.2021.03.017). Briefly, we found that early MIA-exposure was associated with accelerated brain volume increases in adolescence/early-adulthood that normalized in later adulthood, in regions including the striatum, hippocampus, and cingulate cortex. Similarly, alterations in anxiety-like, stereotypic, and sensorimotor gating behaviours observed in adolescence normalized in adulthood. In contrast, MIA-exposure in late gestation had less impact on anatomical and behavioural profiles. </p> <p>In addition to the univariate analyses described above, we also undertook a multivariate analysis (partial least squares) to relate imaging and behavioural variables for the time of greatest alteration, i.e. adolescence/early adulthood. We further explored the molecular underpinnings of region-specific alterations in early MIA-exposed mice in adolescence using RNA sequencing (data for differentially expressed genes in the anterior cingulate cortex, dorsal hippocampus, and ventral hippocampus are available via the original publication https://doi.org/10.1016/j.biopsych.2021.03.017 for a separate cohort of adolescent mice prenatally exposed to MIA or vehicle at GD9). </p> <p>In this dataset, you will find a total of <strong>376 preprocessed structural MRIs</strong> (in MINC format) acquired at postnatal day ~21, ~38, ~60, and ~90 in mice exposed to poly I:C or vehicle control (0.9% sterile saline) at GD9 or 17. These are T1-weighted, manganese enhanced (50mg/kg 24 hours pre-scan), structural images at 100 micron isotropic resolution acquired on a 7 Tesla Bruker Biospec 70/30; matrix size of 180 x 160 x 90; 14.5 minutes, 2 averages, using 5% isoflurane for induction, 1.5% for maintenance of anesthesia during the scan. T1-weighted scans were preprocessed by stripping native coordinates, flipping left-right to maintain fidelity, denoising, correcting inhomogeneities in the bias field using the N4 algorithm, and registering in LSQ6 alignment (i.e. 6 degrees of freedom are allowed for imagine alignment: translations and rotations along x, y, and z dimensions). The demographics information for each animal is included in the <strong>demographics.csv</strong> file. </p> <p>Behavioural tests were performed following the postnatal day 38 and 90 scans in all animals with a 2 day rest period. These include: open field test, marble burying test, three chambered social approach, and prepulse inhibition. The attentional set shifting task was also performed following the final behavioural test in the postnatal day 90 wave of behaviours. The data for all of these tests is presented in its own individual .csv spreadsheet and includes data for both the timepoints evaluated.</p> <p>Included in this data set are the structural MRIs in MINC format, the behavioural .csv data, and a <strong>readme.txt</strong> file providing further detail on the data structure and content, and on how to interpret the data column titles. DICOMS are also available for the structural MRI data, as are the raw (not-preprocessed) MINC files, available upon request to the authors. </p> <p>Finally, the authors would like to acknowledge the funding bodies that supported the completion of this work including the Canadian Institute for Health Research, the Fonds de Recherche du Québec en Santé, and the Healthy Brains for Healthy Lives at McGill University.</p>
Similarity network fusion to identify phenotypes of small for gestational age fetuses
<p>Fetal growth restriction (FGR) affects 5-10% of pregnancies, is the largest contributor to fetal death, and can have long-term consequences for the child. Implementation of a standard clinical classification system is hampered by the multiphenotypic spectrum of small fetuses with substantial differences in perinatal risks. Machine learning and multiomics data can potentially revolutionize clinical decision-making in FGR by identifying new phenotypes. Herein, we describe a cluster analysis of FGR based on an unbiased machine-learning method. Our results <em>confirm</em> the existence of two subtypes of human FGR with distinct molecular and clinical features based on multi-omic analysis. In addition, we demonstrated that clusters generated by machine learning significantly outperform single data subtype analysis and biologically support the current clinical classification in predicting adverse maternal and neonatal outcomes. Our approach can aid in the refinement of clinical classification systems for FGR supported by molecular and clinical signatures. </p>
Gestational Weight and Incentive Research Study
ClinicalTrials.gov study NCT03834194. IPD Sharing: NO. Countries: 1. Publications: 28.
Data from: The evolution of gestation length in eutherian mammals
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Gestational Cd exposure in the CD-1 mouse induces sex-specific hepatic insulin insensitivity, obesity and metabolic syndrome in adult female offspring
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Topological Overlap Matrices for DNA Methylation data of Gestational Diabetes Cohort with BMI and Exposure Status
<p>DNA methylation in placenta was measured with the Infinium HumanMethylation450 BeadChip (Illumina, Inc) microarray, in a sample of 28 women, 20 of whom had a gestational diabetes (GD)-affected pregnancy and 8 who did not. We used GD status as our exposure variable, assuming that this has widespread effects on DNA methylation and on its correlation patterns. Our response, Y, is the standardized body mass index (BMI) in the offspring at the age of 5. For the 10,000 most variable probes, we provide 3 topological overlap matrices (TOM), which are used in our analysis (note that each of the following TOM matrices are a 10,000 by 10,000 symmetric matrix with row names and column names corresponding to the CpG probe IDs:</p> <ol> <li>TOM_Methylation_All_10k.rds: based on all 28 subjects, </li> <li>TOM_Methylation_E0_10k.rds: based on the 8 subjects without a GD-affected pregnancy</li> <li>TOM_Methylation_E1_10k.rds: based on the 20 subjects with a GD-affected pregnancy </li> </ol> <p>The BMI (phenotype) and GD status (exposure) are given in the following dataset:</p> <ol> <li>BMI_and_Exposure_Status.rds: 28 x 2 matrix of the phenotype and exposure. each row is a subject.</li> </ol> <p>Using our ECLUST method (preprint available at http://sahirbhatnagar.com/slides/manuscript1_SB_v4.pdf), we derive 77 clusters, and here we provide the 1st principal component of each cluster:</p> <ol> <li>Cluster_Summary_1stPC.rds: 28 x 77 matrix, where each row is a subject, in the same order as the BMI_and_Exposure_Status.rds data</li> <li>Cluster_CpGs_names.rds: a list of length 77, where each element of the list contains the list of CpG probe IDs contained in each of the clusters</li> </ol> <p>To read in the data use the readRDS function, e.g.:</p> <p>TOM_All <- readRDS(file = "TOM_Methylation_All_10k.rds")</p>
Effects of high dietary zinc supplementation timing on the biological responses of gestating sows and their piglets
<p class="MsoNormal">High dietary zinc (Zn) fed to gestating sows may have utility as a fetal imprinting strategy to decrease pre-weaning mortality of piglets. However, the biological action that Zn may work through is unknown. High Zn may modulate the microbiome of the sow and the microbial seeding of the offspring's gut microbiome. Additonally, high dietary Zn and piglet birth weight may alter gene expression in piglet whole blood. Sows (n = 267) were fed 1 of 3 dietary treatments: 1) Control: a corn-soybean meal-based diet containing 125 ppm total supplemental zinc, 2) Breed-to-Farrow: as Control + 141 ppm supplemental Zn as ZnSO<sub>4 </sub>fed from 5 days post-breeding to farrowing; and 3) Day 110-to-Farrow: as Control + 2,715 ppm supplemental Zn as ZnSO<sub>4 </sub>starting on day 110 of gestation until farrowing. A subset of third parity sows (n = 30) were selected to assess the microbiome of colostrum, milk, and rectal and vaginal surfaces of sows. At farrowing, 4 pigs per litter (n = 120) were selected based on birthweight (BiW), as 2 average BiW pigs and 2 pigs with BiW below the litter average were selected for assessing the piglet gut microbiome on the day of birth (day 0) and day 5 of age. 16S rRNA sequencing were implemented for milk and colostrum samples while all other sample types were sequenced using shotgun metagenomics to determine taxonomic and functional profiles. On a different subset of pigs, whole blood was collected from 9 LBW pigs per treatment and 8 ABW Control pigs for RNA-sequencing to evaluate differentially expressed genes (DEGs) and pathways. Only 2 to 3 genes were differentially expressed between Control LBW and LBW pigs born to sows fed high Zn. However, 262 DEGs were identified when comparing LBW and ABW pigs, mostly reflecting pathways associated with translation, ribosome biogenesis, and amino acid and protein synthesis. Measures of alpha diversity (richness and Shannon's H Index) and beta diversity (Bray-Curtis, PERMANOVA) were conducted along with indicator species analyses. Species with an indicator value of > 0.50 were confirmed with a generalized linear mixed model as each <em>P</em>-value was corrected for false discovery rate (FDR) to generate a Q-value. For piglet samples, the MaAsLin2 R package was used to determine multivariate associations between dietary treatment and piglet BiW. High dietary concentrations of Zn fed to gestating sows did not affect the colostrum, milk, or vaginal microbial diversity or populations of sows. Pathogenic bacteria such as <em>Shigella flexneri </em>and <em>Salmonella enterica</em> were less abundant in fecal samples from Breed-to-Farrow sows compared to Control sows. For piglets born to Breed-to-Farrow sows, their gut microbiome favored fiber fermenting, short chain fatty acid generating microbial species compared to Control pigs. Day 110-to-Farrow piglets demonstrated a lower abundance of SCFA producing bacteria compared to Control piglets. Gene families and pathways playing roles in central metabolic functions (starch, pyruvate, sucrose, amino acid metabolism) were more abundant in Breed-to-Farrow piglets compared to pigs born to Control sows. In conclusion, high Zn fed to gestating sows may influence SCFA-producing species and may reduce the abundance of potential pathogenic bacteria in the sow and piglet. Piglet birth weight may have greater effects on gene expression of neonatal pigs. </p>
Raw data for the association of genetic variants of ErbB4 gene and gestational diabetes mellitus
<div>Gestational diabetes (GDM) is one of the common complications of female pregnancy, which seriously affects the health of patients and their offspring. So far, the etiology has not yet been fully clarified. To clarify the relationship of Erb-b2 receptor tyrosine kinase 4 (ErbB4) genetic variants and GDM risk in a Chinese population, ErbB4 variants (rs1595064, rs1595065, rs1595066 and rs6719645) were selected and genotyped in 554 GDM cases and 641 healthy controls. The associations between variants and GDM risk were evaluated with the odds ratios (ORs) and their corresponding 95% confidence intervals (CIs). The false-positive reporting probability (FPRP), multi-factor dimension reduction (MDR) and bioinformatics analysis were adopted to confirm the significant associations. A nomogram model was constructed to predict the risk of GDM. Association analysis demonstrated that the rs1595066 genotype performed a protective effect on GDM risk among whole subjects. Meanwhile, stratified analysis showed that rs1595066 was significantly associated with GDM risk in various subgroups, such as age>30.09 years old, pre-pregnancy BMI>22.23 Kg/m<sup>2</sup> ,SBP≤110.08 mmHg, etc. Further, interactions between rs1595066 and DBP (Pinteraction=0.01), FPG (Pinteraction<0.001) and HbA1c (Pinteraction< 0.001) were detected. The FPRP analysis confirmed that association of rs1595066 and GDM risk in subjects of FPG≤4.79 mmol/L (P=0.199) is true at a prior probability of 0.1. The MDR analysis suggested that rs1595066 was the best single locus model, while the 4-loci model was considered the best multiple factors model to predict GDM risk. Functional prediction revealed that rs1595066 may disturb the microRNA binding sites to influence the stability of miRNA-mRNA binding. The predictive nomogram model has a good consistency and acceptable discriminative ability with a diagnosed AUC of 0.813.ErbB4 rs1595066 was significantly associated with GDM risk and underlying mechanism causing GDM may be the interaction of gene-gene, gene-environment and the changes in the regulatory effects of miRNAs on ERBB4 expression. The nomogram model has a good prospect for GDM prediction.</div>
Data from: Genetic susceptibility, Mendelian randomization and nomogram model construction of gestational diabetes mellitus
<p>The dataset contains subjects' basic information, including the Identification number of the test sample, fasting plasma glucose (FPG), oral glucose tolerance test 1h plasma glucose (1hPG), oral glucose tolerance test 2h plasma glucose (2hPG), glycated hemoglobin (HbA1c), Systolic blood pressure (SBP), Diastolic blood pressure (DBP), triglyceride (TG), total cholesterol (TC), High-density lipoprotein cholesterol (HDL-c), Low-density lipoprotein cholesterol (LDL-c), and also involves subjects' genetic variant information used for analysis of the association of functional polymorphisms and GDM. The variables including SBP_M, DBP_M, FPG_M, 1hPG_M, 2hPG_M, HbA1c_M, TG_M represent the mean value of SBP, DBP, FPG, 1hPG, 2hPG, HbA1c, TG, which are used for the stratification analysis. This study has obtained the support from the Ethics Committee of Guilin Medical University. All included subjects signed the informed consent.</p>
Impact of maternal obesity on the gestational metabolome and infant metabolome, brain, and behavioral development in rhesus macaques
<p>Maternal gestational obesity is associated with elevated risks for neurodevelopmental disorder, including autism spectrum disorder. However, the mechanisms by which maternal adiposity influences fetal developmental programming remain to be elucidated. We aimed to understand the impact of maternal obesity on the metabolism of both pregnant mothers and their offspring, as well as on metabolic, brain, and behavioral development of offspring by utilizing metabolomics, protein, and behavioral assays in a non-human primate model. We found that maternal obesity was associated with elevated inflammation and significant alterations in metabolites of energy metabolism and one-carbon metabolism in maternal plasma and urine, as well as in placenta. Infants born to obese mothers were significantly larger at birth compared to those born to lean mothers. Additionally, they exhibited significantly reduced novelty preference and significant alterations in their emotional response to stress situations. These changes coincided with differences in phosphorylation of enzymes in the brain mTOR signaling pathway between infants born to obese and lean mothers and correlated with the concentration of maternal plasma betaine during pregnancy. In summary, gestational obesity significantly impacted the infant systemic and brain metabolome and adaptive behaviors.</p>
GCM gelada gestation
<p>Glucocorticoids across gelada gestation</p>
Data of Figure 5 from "Inhibition of IL-1beta improves Glycaemia in a Mouse Model for Gestational Diabetes"
<p>Data of Figure 5 from “Inhibition of IL-1beta improves Glycaemia in a Mouse Model for Gestational Diabetes”</p> <p>Dataset (doi: 10.1038/s41598-020-59701-0) contains the original publication as PDF-format (10.1038_s41598-020-59701-0). Corresponding raw data obtained from LC-MS/MS analysis provided as two files in CSV format (31003A-179400_10.1038_s41598-020-59701-0_DW_4-1.csv, 31003A-179400_10.1038_s41598-020-59701-0_DW_4-2.csv). All further experiment related information provided as three meta-data-files (31003A-179400_10.1038_s41598-020-59701-0_DW _4-1_M_1.PDF, 31003A-179400_10.1038_s41598-020-59701-0_DW _4-2_M_1.PDF, 31003A-179400_10.1038_s41598-020-59701-0_DW _4_1-2_M_2.pdf) as PDF format.</p>
Saliva and plasma metabolome analysis in mares during anestrus, estrus cycle and early gestation for the identification of salivary biomarkers of reproductive stages.
<p>1H-NMR spectra of saliva and blood samples collected at seven physiological stages from six pony mares:</p> <ul> <li>in seasonal anestrus,</li> <li>in the follicular phase 3 days, 2 days and 1 day before ovulation, and the day when ovulation was detected,</li> <li>in the luteal phase 6 days after ovulation,</li> <li>in gestation 18 days after ovulation and artificial insemination.</li> </ul> <p> </p> <p>The 42 saliva samples were prepared for <sup>1</sup>H-NMR by precipitation of proteins using methanol. Briefly, 200 µL of saliva was mixed with 400 µL of cold methanol and vortexed. The mixtures were cooled at -20°C for 20 min before centrifugation at 15,000 × g for 15 min at 4°C. The supernatants were recovered and transferred to glass tubes for further evaporation of the solvent. For the 42 plasma samples, a modified Folch’s method (200 µL of plasma, 300 µL of cold methanol and 500 µL of cold chloroform) was preferred to extract metabolites and eliminate proteins and lipids from the plasmas in order to avoid the overlapping of the metabolites of interest with broad lipid and protein signals. The samples were vortexed during 1 min. The polar fractions, containing the metabolites, were separated after centrifugation at 15,000 × g for 15 min at 4°C and 300 µL of the samples were collected in glass tubes. The solvent of saliva supernatants and plasma polar fractions were evaporated in a SpeedVac (Thermo Fisher Scientific, Illkirch-Graffenstaden, France) for 2 h at 35°C followed by another 2 h at room temperature before storage at -20°C until analysis. Five quality control samples for the saliva and plasma experiments were prepared by pooling a fraction of each samples (either saliva or plasma) and were further processed with all the other samples.</p> <p>Before <sup>1</sup>H-NMR analyses, the dried residues were recovered in 210 μL phosphate buffer (pH 7.4, 200 mM) prepared in D<sub>2</sub>O supplemented with 152 µM (final concentration) of 3-trimethylsilylpropionic acid (TSP) as internal reference and transferred to 3 mm NMR tubes.</p> <p><sup>1</sup>H-NMR spectra of the saliva and plasma samples were acquired at 298K on an AVANCE III HD 600 MHz system (Bruker Biospin, Karlsruhe, Germany) equipped with a Bruker 5 mm TCI CryoProbe with Z-gradient. <sup>1</sup>H-NMR spectra were recorded with the «noesypr1d» pulse sequence with a relaxation delay of 20 s, on a sweep width of 12 ppm, 64 k data points, an acquisition time of 4.56 s, with 64 transients, and 8 dummy scans. Sample shimming was performed automatically on the D<sub>2</sub>O signal.</p>
The Effects of Aspirin in Gestation and Reproduction
ClinicalTrials.gov study NCT00467363. IPD Sharing: Not stated. Countries: 1. Publications: 42.
Early Gestational Diabetes Screening in the Gravid Obese Woman
ClinicalTrials.gov study NCT01864564. IPD Sharing: NO. Countries: 1. Publications: 1.
Genotropin Treatment In Very Young Children Born Small For Gestational Age
ClinicalTrials.gov study NCT00627523. IPD Sharing: Not stated. Countries: 9. Publications: 1.
Comparison of Two Screening Strategies for Gestational Diabetes (GDM2)
ClinicalTrials.gov study NCT02309138. IPD Sharing: YES. Countries: 1. Publications: 3.
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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.
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.