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Synaptic dysfunction underlies many neurodevelopmental disorders (NDDs). The membrane-associated mucin domain-containing glycosylphosphatidylinositol anchor proteins (MDGAs) regulate synaptic development by modulating neurexin–neuroligin complex formation. Since understanding the neurodevelopmental profile and the sex-based differences in the manifestation of the symptoms of NDDs is important for their early diagnosis, we tested a mouse model haploinsufficient for MDGA2 (MDGA2+/-) on a neurodevelopmental test battery, containing sensory, motor, and cognitive measures, as well as ultrasonic vocalizations. When male and female MDGA2+/- and wildtype (WT) C57BL/6 J mice were examined from 2 to 23 days of age using this test battery, genotype and sex differences in body weight, sensory-motor processes, and ultrasonic vocalizations were observed. The auditory startle reflex appeared earlier in the MDGA2+/- than in WT mice and the MDGA2+/- mice produced fewer ultrasonic vocalizations. The MDGA2+/- mice showed reduced locomotion and rearing than WT mice in the open field after 17 days of age and spent less time investigating a novel object than WT mice at 21 days of age. Female MDGA2+/- mice weighed less than WT females and showed lower grip strength, indicating a delay in sensory-motor development in MDGA2+/- mice, which appears to be more pronounced in females than males. The behavioural phenotypes resulting from MDGA2 haploinsufficiency suggests that it shows delayed development of motor behaviour, grip strength and exploratory behaviour, non-social phenotypes of NDDs.

Additional file 7. Table S7: P values and regression coefficients for the correlation between DNA methylation in blood with four brain regions (prefrontal cortex, entorhinal cortex, superior temporal gyrus and cerebellum) from 71 to 75 matched samples for all the 8 CpG probes. The data are taken from the Blood Brain DNA Methylation Comparison Tool [17].

Representative flow cytometry plots of 3 pitutiary adenoma samples showing Sox2 and CD15 expression. (TIFF 791 kb)

Fold change (FC ≤ 1.5) list and GO enrichment analysis of probes affected by IHNV status.

OBJECTIVE. To assess whether HS severity is mirrored at the level of large-scale networks. METHODS. We studied preoperative high-resolution anatomical and diffusion-weighted MRI of 44 TLE patients with histopathological diagnosis of HS (n=25; TLE-HS) and isolated gliosis (n=19; TLE-G), and 25 healthy controls. Hippocampal measurements included surface-based subfield mapping of atrophy and T2 hyperintensity indexing cell loss and gliosis, respectively. Whole-brain connectomes were generated via diffusion tractography and examined using graph theory along with a novel network control theory paradigm which simulates functional dynamics from structural network data. RESULTS. Compared to controls, we observed markedly increased path length and decreased clustering in TLE-HS compared to controls, indicating lower global and local network efficiency, while TLE-G showed only subtle alterations. Similarly, network controllability was lower in TLE-HS only, suggesting limited range of functional dynamics. Hippocampal imaging markers were positively associated with macroscale network alterations, particularly in ipsilateral CA1-3. Systematic assessment across several networks revealed maximal changes in the hippocampal circuity. Findings were consistent when correcting for cortical thickness, suggesting independence from grey matter atrophy. CONCLUSIONS. Severe HS is associated with marked remodeling of connectome topology and structurally-governed functional dynamics in TLE, as opposed to isolated gliosis which has negligible effects. Cell loss, particularly in CA1-3, may exert a cascading effect on brain-wide connectomes, underlining coupled disease processes across multiple scales. Data_phen_conn_dryadPhenotypic information and mean connectome feature data for Bernhardt et al. (2019) Temporal lobe epilepsy: hippocampal pathology modulates white matter connectome topology and controllability. Neurology

Multivariate structural MRI templates and quantitative atlases from multi-echo T2 relaxation (GRASE images, MWF quantitative maps) and steady-state (mcDESPOT/IRSPGR images, fM quantitative maps) myelin water imaging approaches, along with regions of interest generated and analyzed for Myelin imaging in the central nervous system: Comparison of multi-echo T2 relaxation and steady-state approaches

This dataset contains synthetic data from simulations (for a total duration of 10 minutes) including the activity of one multi-unit and two single-units for different firing rates and signal-to-noise ratio levels. It is intended to be used as a standardized dataset to evaluate spike sorting algorithms. Recordings were taken using a sampling rate of 24 kHz, and are comprised of spikes from a database with 594 different average spike shapes, taken from real recordings from monkey neocortex and basal ganglia. This dataset is comprised of two files: data.npy and labels.csv. data.npy contains 14,400,000 sampled voltage values, from a single channel, taken at a sampling rate of 24 kHz. labels.csv contains the timestep, spike class, amplitude (SNR), and firing rate associated with each spiking event. The original samples used to construct this dataset where previously constructed and made available in [1]. This dataset is an amalgamation of simulation files, which were previously publicly accessible at: http://www2.le.ac.uk/departments/engineering/research/bioengineering/neuroengineering-lab/software. Consequently, when using or making modifications to this dataset, in addition to acknowledging this record, [1] must also be acknowledged, as per the original author's request. [1] J. Martinez, C. Pedreira, M. J. Ison, and R. Quian Quiroga, ���Realistic simulation of extracellular recordings,��� Journal of Neuroscience Methods, vol. 184, no. 2, pp. 285���293, Nov. 2009, doi: 10.1016/j.jneumeth.2009.08.017. {"references": ["J. Martinez, C. Pedreira, M. J. Ison, and R. Quian Quiroga, \"Realistic simulation of extracellular recordings,\" Journal of Neuroscience Methods, vol. 184, no. 2, pp. 285\u2013293, Nov. 2009, doi: 10.1016/j.jneumeth.2009.08.017."]}

Abstract Multiple studies have corroborated the restoration of volitional motor control after motor-complete spinal cord injury (SCI) through the use of epidural spinal cord stimulation (eSCS), but rigorous quantitative descriptions of muscle coordination have been lacking. Six participants with chronic, motor and sensory complete SCI underwent a brain motor control assessment (BMCA) consisting of a set of structured motor tasks with and without eSCS. We investigated how muscle activity complexity and muscle synergies changed with and without stimulation. We performed this analysis to better characterize the impact of stimulation on neuromuscular control. We also recorded data from nine healthy participants as controls. Competition exists between the task origin and neural origin hypotheses underlying muscle synergies. The ability to restore motor control with eSCS in participants with motor and sensory complete SCI allows us to test whether changes in muscle synergies reflect a neural basis in the same task. Muscle activity complexity was computed with Higuchi Fractal Dimensional (HFD) analysis, and muscle synergies were estimated using non-negative matrix factorization (NNMF) in six participants with American Spinal Injury Association (ASIA) Impairment Score (AIS) A. We found that the complexity of muscle activity was immediately reduced by eSCS in the SCI participants. We also found that over the follow-up sessions, the muscle synergy structure of the SCI participants became more defined, and the number of synergies decreased over time, indicating improved coordination between muscle groups. Lastly, we found that the muscle synergies were restored with eSCS, supporting the neural hypothesis of muscle synergies. We conclude that eSCS restores muscle movements and muscle synergies that are distinct from those of healthy, able-bodied controls.

Numerous studies have been performed to examine gene expression patterns in the rodent hippocampus in the kindling model of epilepsy. However, recent reviews of this literature have revealed limited agreement among studies. Because this conclusion was based on retrospective comparison of reported "hit lists" from individual studies, we hypothesized that re-analysis of the original expression data would help address this concern. In this paper, we reanalyzed four genome-wide expression studies of excitotoxin-induced kindling in rat and performed a statistical meta-analysis. The meta-analysis revealed over 800 genes which show significant change in expression 24 h after initial seizure induction, and 59 genes altered after 10 days. To evaluate our results in light of previous work, we assembled a reference list of genes formed from a consensus of the published literature. Our profiles include most of the genes in this reference list, and most of the additional genes are from pathways or biological processes previously recognized to be altered in kindling. In addition our results emphasized expression changes in lipid metabolism and protein degradation pathways. We conclude that a cautious re-analysis of published expression data can help illuminate genes and pathways underling kindling. Supplementary Material is available at http://www.chibi.ubc.ca/faculty/pavlidis/meta-analysis-of-brain-kindling/. http://hdl.handle.net/11272/10553