Differential effects of early or late exposure to prenatal maternal immune activation on mouse embryonic neurodevelopment

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. 

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.

In this dataset, you will find a total of 187 preprocessed structural MRIs (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).

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 demographics.csv file. 

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 EM_raw_data_per_slice.csv and EM_average_per_mouse.csv files. 

Included in this data set are the structural MRIs in MINC format, corresponding demographics information (demographics.csv), electron microscopy data from the dorsal hippocampus (EM_raw_data_per_slice.csv and EM_average_per_mouse.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.The raw (not-preprocessed) MINC files, as well as MINC files cropped to the head of the embryos available upon request to the authors. 

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.