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44 results for “maternal immune activation”
Differential effects of early or late exposure to prenatal maternal immune activation on mouse embryonic neurodevelopment
<p>Exposure to maternal immune activation (MIA) in utero is a risk factor for neurodevelopmental and psychiatric disorders. MIA-induced deficits in adolescent and adult offspring have been well characterized, however, less is known about the effects of MIA-exposure on embryo development. To address this gap, we collected high-resolution ex vivo magnetic resonance imaging (MRI) of C57BL/6 mouse embryos (gestational day [GD]18) who were prenatally exposed to MIA either early (GD9) or late (GD17) in gestation. We further examined hippocampal neuroanatomy using electron microscopy and identified differential effects due to MIA-timing. </p> <p>The data published here was collected and analyzed for the following publication available as a preprint on BioRxiv (https://www.biorxiv.org/content/10.1101/2021.07.14.452084v2). Briefly, We identify striking neuroanatomical changes in the embryo brain, particularly in the late exposed offspring. An increase in apoptotic cell density was observed in the GD9 exposed offspring, while an increase in the density of dark neurons and glia, putative markers for increased neuroinflammation and oxidative stress, was observed in GD17 exposed offspring, particularly in females. Overall, our findings integrate imaging techniques across different scales to identify differential impact of MIA-timing on the earliest stages of neurodevelopment.</p> <p>In this dataset, you will find a total of <strong>187 preprocessed structural MRIs </strong>(in MINC format) of whole embryos at gestational day 18. These embryos were exposed to poly I:C or vehicle control (0.9% sterile saline) at GD9 or 17. A multi-channel 7.0-T MRI scanner with a 40 cm diameter bore (Varian Inc., Palo Alto, CA), with a custom-built 16-coil solenoid array was used to acquire T2-weighted, gadolinium enhanced structural images at 40 μm3 resolution images from 16 samples concurrently (3D fast spin echo sequence using a cylindrical k-space acquisition; TR/TE=350/12 ms, echo train length=6, two averages, field-of-view 20 mm x 20 mm x 25 mm, matrix size=504 x 504 x 630).</p> <p>An N4 correction for B1 bias field inhomogeneities and denoising using non-local means (minc_anlm) was applied to the T2-weighted images, and the background was set to zero using minc tools. The demographics information for each animal is included in the <strong>demographics.csv</strong> file. </p> <p>The dorsal hippocampus was selected as a region of interest in which the total number and density of total cells, dark neurons, dark glia, apoptotic cells were assessed (as presented in our manuscript). This is available in the <strong>EM_raw_data_per_slice.csv</strong> and <strong>EM_average_per_mouse.csv </strong>files. </p> <p>Included in this data set are the <strong>structural MRIs in MINC format</strong>, corresponding demographics information (<strong>demographics.csv</strong>), electron microscopy data from the dorsal hippocampus (<strong>EM_raw_data_per_slice.csv</strong> and <strong>EM_average_per_mouse.csv)</strong> 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.The raw (not-preprocessed) MINC files, as well as MINC files cropped to the head of the embryos 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>
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>
Investigating the "two-hit hypothesis": effects of prenatal maternal immune activation and adolescent cannabis use on neurodevelopment in mice
<p>Prenatal exposure to maternal immune activation (MIA) and chronic adolescent cannabis use have both been identified as environmental risk factors for neuropsychiatric disorders. However, most individuals exposed to a single risk factor do not typically develop major mental illness, which suggests that multiple exposures may be required for illness onset. Here, we examine whether combined exposure to prenatal MIA and adolescent delta-9-tetrahydrocannabinol (THC), the main psychoactive component of cannabis, lead to enduring neuroanatomical and behavioural changes in adult offspring, potentially reflecting changes in humans indicative of mental illness. </p> <p>Mice were prenatally exposed to a viral mimetic, poly I:C (5mg/kg), or vehicle at gestational day (GD)9, and then postnatally exposed to chronic THC (5mg/kg) or vehicle by intraperitoneal injections during adolescent development (postnatal day [PND]28-45). Longitudinal in vivo whole-brain magnetic resonance imaging (MRI) was performed pre-treatment, PND25, post-treatment, PND50, and in adulthood, PND85, followed by a series of behavioural tests aimed at assessing anxiety-like and locomotor, social, and sensorimotor gating behaviour. Post-mortem assessment of cannabinoid (CB)1 and 2 receptor expressing cells was performed in developmentally altered regions identified by MRI (anterior cingulate and somatosensory cortices, striatum, and hippocampus). We hypothesized that there would be differential, but synergistic effects of each exposure.</p> <p>Briefly, we found subtle deviations in neurodevelopmental trajectory and subthreshold anxiety-like behaviours were observed in mice exposed to both risk factors. Sex-dependent effects were observed in patterns of shared brain-behaviour covariation, suggesting that exposure to MIA and THC may affect males and females in different ways. Density of CB1 and CB2 receptor positive cells was significantly decreased in all regions assessed for all mice exposed to either one or both risk factors, relative to controls.</p> <p>These findings suggest that there may be a cumulative effect of risk factor exposure on gross neuroanatomical and behavioural development, and that the endocannabinoid system may be sensitive to both prenatal MIA, adolescent THC, or the combination. For full details, see our publication: .</p> <p>In this dataset, you will find a total of 243 preprocessed structural MRIs (in MINC format) acquired at postnatal day ~25, ~50, and ~85 in mice exposed to poly I:C or vehicle control (0.9% sterile saline) at GD9, and then postnatally treated with vehicle or THC from PND 28-45. These are T1-weighted 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, 20 degrees and TE/TR of 4.5/20 ms (2 averages, ~14 minutes). Anesthesia was induced with 3% isoflurane in oxygen and a (0.075 mg/kg bolus) dexmedetomidine injection. Anesthesia was maintained during the scan between 1.5-0.5% isoflurane, and a constant infusion of dexmedetomidine (0.05mg/kg/h continuous mg/kg during 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 demographics.csv file. </p> <p>Behavioural tests were performed following the postnatal day 85 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 its own individual .csv spreadsheet.</p> <p>Included in this data set are the structural MRIs in MINC format, the behavioural .csv data, and a readme.txt 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>
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>
Subtle alterations in neonatal neurodevelopment following early or late exposure to prenatal maternal immune activation
<p>Structural MRI</p>
The fetal programming effect of maternal immune activation (MIA) on the offspring's immune system.
<h2>Online dataset: Cytokine profile of maternal immune activation (MIA) offspring</h2> <p>In preclinical animal maternal immune activation (MIA) models, alterations in the cytokine profiles were reported for MIA exposed offspring. This <strong>online dataset</strong> is a searchable spreadsheet provinding a more thorough summary of the cytokine profile observed in MIA exposed offspring. It includes the analyzed cytokines, the utilized animal model, age of the offspring and the specific tisssue/sample used from multiple studies.</p> <p>NA; Not affected -; not detected</p>
Impact of Maternal Immune Activation and Sex on Placental and Fetal Brain Cytokine and Gene Expression Profiles in a Preclinical Model of Neurodevelopmental Disorders
GEO Series GSE248222. Mus musculus. 64 samples. Type: Expression profiling by high throughput sequencing.
Gene expression profile on pons and medulla of maternal immune activation model rat
GEO Series GSE296396. Rattus norvegicus. 4 samples. Type: Expression profiling by array.
tRNA-derived fragments and microRNAs in the maternal-fetal interface of a mouse maternal-immune-activation autism model
GEO Series GSE139191. Mus musculus. 84 samples. Type: Non-coding RNA profiling by high throughput sequencing.
Sex differences in offspring risk and resilience following 11β-hydroxylase antagonism in a rodent model of maternal immune activation
GEO Series GSE240604. Rattus norvegicus. 23 samples. Type: Expression profiling by high throughput sequencing.
A temporal map of maternal immune activation-induced changes reveals a shift in neurodevelopmental timing and perturbed cortical development in mice
GEO Series GSE166376. Mus musculus. 74 samples. Type: Expression profiling by high throughput sequencing.
The placenta has an active role in maintaining fetal homeostasis following maternal immune activation
GEO Series GSE224116. Mus musculus. 413 samples. Type: Expression profiling by high throughput sequencing.
Maternal Immune Activation perturbs fetal hematopoietic development and causes persistent changes to postnatal immunity [scRNA-Seq']
GEO Series GSE161926. Mus musculus. 6 samples. Type: Expression profiling by high throughput sequencing.
Early or Late Gestational Exposure to Maternal Immune Activation Alters Neurodevelopmental Trajectories in Mice: An Integrated Neuroimaging, Behavioral, and Transcriptional Study
GEO Series GSE178403. Mus musculus. 72 samples. Type: Expression profiling by high throughput sequencing.
Maternal Immune Activation perturbs fetal hematopoietic development and causes persistent changes to postnatal immunity [RNA-Seq]
GEO Series GSE161925. Mus musculus. 4 samples. Type: Expression profiling by high throughput sequencing.
Alternative splicing Hltf: intron retention-dependent activation of immune tolerance at the feto-maternal interface
GEO Series GSE114146. Mus musculus. 16 samples. Type: Expression profiling by high throughput sequencing; Methylation profiling by high throughput sequencing.
Evaluation of the effect of maternal immune activation and weaning on hypothalamus of 22 day old pigs
GEO Series GSE227725. Sus scrofa. 73 samples. Type: Expression profiling by high throughput sequencing.
Microglial transcriptome of Maternal Immune Activation model at different developmental Stages and after microglia repopulation
GEO Series GSE146526. Mus musculus. 30 samples. Type: Expression profiling by high throughput sequencing.
Maternal immune activation elicits rapid and sex-dependent changes in gene expression and vascular dysfunction in the rat placenta
GEO Series GSE272437. Rattus norvegicus. 16 samples. Type: Expression profiling by high throughput sequencing.
Maternal Immune Activation imprints translational dysregulation and differential MAP2 phosphorylation in descendant neural stem cells
GEO Series GSE278057. Mus musculus. 12 samples. Type: Expression profiling by high throughput sequencing.
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