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opencc-by-4.0May 2022View details →

Data and code for Barrett, Martin, and Shepherd (2022) "Manipulation-specific cortical activity as mice handle food"

This dataset contains the tracking data, spiking data, and ethograms necessary to reproduce the results of Barrett, Martin, and Shepherd (2022) "Manipulation-specific cortical activity as mice handle food". Also included is Matlab and R code that generates all of the figures, tables, and stats in the aforementioned paper.

opencc-by-4.0Mar 2022View details →

Investigating the "two-hit hypothesis": effects of prenatal maternal immune activation and adolescent cannabis use on neurodevelopment in mice

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.  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. 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. 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: . 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.  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. 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.  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.

dryad40/100

Data from: Single cell transcriptomics shows dose-dependent disruption of hepatic zonation by TCDD in mice

2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) dose-dependently induces the development of hepatic fat accumulation and inflammation with fibrosis in mice initially in the portal region. Conversely, differential gene and protein expression is first detected in the central region. To further investigate cell-specific and spatially resolved dose-dependent changes in gene expression elicited by TCDD, single-nuclei RNA sequencing and spatial transcriptomics were used for livers of male mice gavaged with TCDD every 4 days for 28 days. The proportion of 11 cell (sub)types across 131,613 nuclei dose-dependently changed with 68% of all portal and central hepatocyte nuclei in control mice being overtaken by macrophages following TCDD treatment. We identified 368 (portal fibroblasts) to 1,339 (macrophages) differentially expressed genes. Spatial analyses revealed initial loss of portal identity that eventually spanned the entire liver lobule with increasing dose. Induction of R-spondin 3 (Rspo3) and pericentral Apc, suggested dysregulation of the Wnt/β-catenin signaling cascade in zonally resolved steatosis. Collectively, the integrated results suggest disruption of zonation contributes to the pattern of TCDD-elicited NAFLD pathologies.

opencc-zeroOct 2022View details →

Fig. 7. a in Anti-cryptosporidial activity of Camellia sinensis (green tea extract) in experimentally infected immunocompromised mice

Fig. 7. a) A section of the small intestine in GV revealed normal villous architecture with a normal brush border (H&E stain, X200); b) Sections examined from the liver in this group showed preserved hepatic lobular architecture (H&E stain, X200).

Fig. 6. a in Anti-cryptosporidial activity of Camellia sinensis (green tea extract) in experimentally infected immunocompromised mice

Fig. 6. a) A section of the small intestine in GIV revealed marked villous broadening (red line) with decreased villous height to crypt length ratio. There was dense infiltration by mononuclear inflammatory cells within the villous core (green arrows), degeneration of the villous tip-regions (black arrows), and increased mucin production (H&E stain, X200). b) Sections from the small intestine revealed many adherents (red arrows) and separate (black arrows) Cryptosporium stages, probably oocyst (H&E stain, X1000). c)Sections examined from the liver in this group showed hepatocellular degeneration (black arrow) and focal mononuclear cellular infiltration (red arrows) (H&E stain, X200)

Fig. 5. a in Anti-cryptosporidial activity of Camellia sinensis (green tea extract) in experimentally infected immunocompromised mice

Fig. 5. a) A section of the small intestine in GIII revealed moderate villous broadening, infiltration by mononuclear inflammatory cells within the villous core (red arrow), focal degeneration of the villous tip regions (black arrow), and increased mucin production (H&E stain, X200). b) Sections examined from the liver in this group showed focal mononuclear cellular infiltration (red arrow) (H&E stain, X200).

Fig. 3. a in Anti-cryptosporidial activity of Camellia sinensis (green tea extract) in experimentally infected immunocompromised mice

Fig. 3. a) A section of the small intestine in GI revealed villous broadening (red line) with an expansion of the villous core by mononuclear inflammatory cells (black arrow) (H&E stain, X200); b) Sections examined from the liver in this group showed preserved hepatic lobular architecture and cloudy swelling of hepatocytes (H&E stain, X200).

Fig. 1. a in Anti-cryptosporidial activity of Camellia sinensis (green tea extract) in experimentally infected immunocompromised mice

Fig. 1. a) Cryptosporidium oocyst (stained red to deep purple with the modified Ziehl–Neelsen method); b) immunofluorescence staining of Cryptosporidium oocyst (ovoid or spherical brilliant apple/ green structure)

Fig. 2 in Anti-cryptosporidial activity of Camellia sinensis (green tea extract) in experimentally infected immunocompromised mice

Fig. 2. Agarose gel electrophoresis showing: Lane 1: 50 bp DNA molecular weight marker, Lane 2: Positive control, Lane 3: Negative control, Lane 4: Positive sample of nested PCR products targeting COWP gene of Cryptosporidium at 553 bp, Lane 5: 50 bp DNA molecular weight marker, and Lane 6: RFLP products of the sample after digestion with RsaI endonuclease (C. parvum genotype 2 digestion products at 410, 106, and 34 (too small to be detected) bp.

Fig. 4. a in Anti-cryptosporidial activity of Camellia sinensis (green tea extract) in experimentally infected immunocompromised mice

Fig. 4. a) A section of the small intestine in GII revealed returning of the normal villous pattern, normal mucosa, and goblet cells (H&E stain, X200). b) Sections examined from the liver in this group showed preserved hepatic lobular architecture (H&E stain, X200).

opencc-by-4.0Jun 2024View details →

Diet-microbiome interactions following spinal cord injury in mice

Here, we performed 16S (V3-V4) rRNA sequencing of the stool microbiome in mice following spinal cord injury, with or without a dietary fiber intervention. Provided here are two .zip files containing the downstream analyses of two independent cohorts (both experimentally and in sequencing/analysis), as performed by Zymo, Inc through their Microbiomics platform. Each .zip file contains a "Report" HTML file which summarizes key findings. All underlying data for each analysis are included in sub folders, inclusive of taxonomic composition and various diversity measurements. Sequences used in these analyses have been deposited into the NCBI SRA database under accession #PRJNA1119045.

opencc-by-4.0Dec 2015View details →

Fig. 3 in SjTat-TPI facilitates adaptive T-cell responses and reduces hepatic pathology during Schistosoma japonicum infection in BALB/c mice

Fig. 3 Th1 immune response acter CD8+T cells blockage in sitro. a. CD3+CD8+T cells were successcullv blocked. The blocking ecciciencv was more than 99.6 %. b, c. Percentages oc CD4+IFN-γ+ (Th1) in Tat-TPI (T-TPI), TPI stimulated splenocvtes with or without CD8+T-cell blockage. Data are presented as the means ± SEM crom cour independent experiments. (*P <0.05; **P <0.01)

Fig. 4 in Angiostrongylus cantonensis induces energy imbalance and dyskinesia in mice by reducing the expression of melanin-concentrating hormone

Fig. 4 AC infection causes imbalance in GLU and lipid metabolism in mice. A Serum biochemical tests (n = 6), including GLU, CHO, TG, HDL, LDL. B, C GLU tolerance and AUC curve (n = 3). D, E Immunohistochemical images and statistics of UCP1 in mouse gWAT (n = 3). Data are presented as mean ± SD. Compared with the control group, statistical significance is indicated as *P <0.05, **P <0.01, ***P <0.001, ****P <0.0001. GLU glucose, TG triglycerides, LDL low-density lipoprotein, HDL high-density lipoprotein, TC total cholesterol, AUC area under the curve

Fig. 3 in Angiostrongylus cantonensis induces energy imbalance and dyskinesia in mice by reducing the expression of melanin-concentrating hormone

Fig. 3 AC infection leads to extensive loss of adipose tissue in mice. A Macroscopic images. B, C, D Statistical chart of tissue weight proportion to body weight in different parts (n = 6). E Pathological sections of adipose tissue. F, G Statistical chart of the average single-cell area of iWAT and gWAT (n = 3). Data are presented as mean ± SD. Compared with the control group, statistical significance is denoted as *P <0.05, **P <0.01, ****P <0.0001. BAT brown adipose tissue, iWAT inguinal white adipose tissue, gWAT gonadal white adipose tissue

Fig. 8 in Angiostrongylus cantonensis induces energy imbalance and dyskinesia in mice by reducing the expression of melanin-concentrating hormone

Fig. 8 Effect of intranasal MCH on synapse-related proteins. A Transcription levels of Bcl2, Map2, PSD95, Syp in mouse cortex (n = 5). B The expression levels of MAP2, PSD95, and SYP were evaluated by western blotting. C Densitometrical quantification of the blots after normalizing with β-actin (n = 3). Data are presented as mean ± SD. Compared with the AC group, statistical significance is indicated as *P <0.05, **P <0.01. Bcl2 B cell leukemia/lymphoma 2, Map2 microtubule-associated protein 2, PSD95 postsynaptic density protein 95, Syp Synaptophysin, AC Angiostrongylus cantonensis, MCH melanin-concentrating hormone

Fig. 1 in Angiostrongylus cantonensis induces energy imbalance and dyskinesia in mice by reducing the expression of melanin-concentrating hormone

Fig. 1 AC infection reduces MCH expression in mice. A Differential volcano plot illustrating brain transcriptome changes in AC-infected mice. B RT– qPCR analysis of Pmch mRNA transcription levels in the whole brain (n = 3) and hypothalamus (n = 4). C, D Panoramic localization of MCH in coronal brain sections. Part D is an enlarged view of part C. E, F Representative images of MCH costained with NeuN and GFAP. G, H Representative images depicting MCH immunofluorescence in hypothalamic regions, along with fluorescence intensity statistics (n = 3). Data are presented as mean ± SD. Compared with the control group, statistical significance is denoted as *P <0.05, ****P <0.0001. NotSig not significant, Pmch pro-melanin-concentrating hormone, dpi days post infection, MCH melanin-concentrating hormone, DAPI 4′,6-diamidino-2-phenylindole, NeuN neuronal nuclei, GFAP glial fibrillary acidic protein, 3V 3rd ventricle, ARH hypothalamic arcuate nucleus, DMH dorsomedial hypothalamus, LHA lateral hypothalamic area, VMH ventromedial hypothalamic nucleus, ZI zona incerta

Fig. 5 in Angiostrongylus cantonensis induces energy imbalance and dyskinesia in mice by reducing the expression of melanin-concentrating hormone

Fig. 5 AC infection causes neurological impairment and dyskinesia in mice. A Neurological function score (n ≥ 4). B MWM trajectory. C, D, E, F Statistics of platform crossings, percentage time in target quadrant, distance, and velocity in MWM (n ≥ 4). G, H Changes in running wheel activity and statistics (n ≥ 5). Data are presented as mean ± SD. Compared with the control group, statistical significance is indicated as *P <0.05, **P <0.01, ***P <0.001, ****P <0.0001. dpi days post infection

Fig. 7 in Angiostrongylus cantonensis induces energy imbalance and dyskinesia in mice by reducing the expression of melanin-concentrating hormone

Fig. 7 MCH improves neurological function and dyskinesia in mice. A Y-maze movement trajectory. B, C, D Statistics of Y-maze free alternation rate, distance, and velocity (n ≥ 6). E NOR test trajectory. F, G, H Statistics of recognition index, mouse travel distance, and velocity in NOR test (n ≥ 5). I MWM movement trajectory. J, K, L, M Statistics of platform crossings, percentage time in target quadrant, distance, and velocity in MWM (n ≥ 5). N Statistics of the time spent in the pole test (n = 4). O Neurological function score (n = 6). Data are presented as mean ± SD. Compared with the AC group, statistical significance is indicated as *P <0.05, **P <0.01, ***P <0.001, ****P <0.0001. AC Angiostrongylus cantonensis, MCH melanin-concentrating hormone

opencc-by-4.0Dec 2015View details →

Fig. 2 in SjTat-TPI facilitates adaptive T-cell responses and reduces hepatic pathology during Schistosoma japonicum infection in BALB/c mice

Fig. 2 Immune responses in the draining popliteal lvmph nodes oc mice induced bv Tat-TPI (T-TPI) and TPI proteins. a and c. Percentages oc CD4+IFN-γ+ cells (Th1), CD8+IFN-γ+ cells (Tc1) analvsed bv FACS. b. The ratio oc CD4+ T cells to CD8+ T cells (CD4/CD8) in the draining popliteal lvmph nodes. Data are presented as the means ± SEM crom six mice in each group. (*P <0.05; **P <0.01)