Brain Anatomy 3d Model Free Download

This interactive brain model is powered by the Wellcome Trust and developed by Matt Wimsatt and Jack Simpson; reviewed by John Morrison, Patrick Hof, and Edward Lein.

Structure descriptions were written by Levi Gadye and Alexis Wnuk and Jane Roskams.

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Although neurons attract the most attention in neurobiology, our current knowledge of neural circuit can only partially explain the neurological and psychiatric conditions of the brain. Thus, it is also important to consider the influence of brain interstitial system (ISS), which refers to the space among neural cells and capillaries. The ISS is the major compartment of the brain microenvironment that provides the immediate accommodation space for neural cells, and it occupies 15% to 20% of the total brain volume. The brain ISS is a dynamic and complex space connecting the vascular system and neural networks and it plays crucial roles in substance transport and signal transmission among neurons. Investigation of the brain ISS can provide new perspectives for understanding brain architecture and function and for exploring new strategies to treat brain disorders. This review discussed the anatomy of the brain ISS under both physiological and pathological conditions, biophysical modeling of the brain ISS and in vivo measurement and imaging techniques, including recent findings on brain ISS divisions. Moreover, the implications of ISS knowledge for basic neuroscience and clinical applications are addressed.

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A mouse model with a deletion in exon 52 of the Dmd gene, the mdx52 mouse (Araki et al., 1997), is an interesting model for preclinical studies addressing both muscular and CNS dysfunctions, as it is deficient in both Dp427 and Dp140. Although mdx52 mice display clear and typical muscular dysfunctions, their behavioral disturbances need to be characterized. The mdx52 mice are expected to display at least comparable cognitive and behavioral deficits as the ones observed in the original mdx mouse lacking Dp427. However, the impact of the additional loss of Dp140 in mdx52 mice is unknown and might influence the severity and/or nature of the central deficits. The cellular function of Dp140 is largely unknown (Lidov et al., 1995) but its higher expression in fetal brain compared to adult brain (Morris et al., 1995) suggests that its loss might affect fetal brain formation and development. Importantly, it has been shown that exon-skipping strategies based on intracerebral or systemic administration of antisense sequences are efficient at skipping exon 23 to restore the reading frame and partially re-express Dp427 in the brain of mdx mice, thereby improving GABAergic functions, synaptic plasticity and behavioral fear responses in this model (Dallrac et al., 2011; Goyenvalle et al., 2015; Vaillend et al., 2010). Recent studies demonstrated that the mdx52 mouse is also eligible for exon-skipping strategies using systemic administration of naked or vectorized antisense sequences to skip exon 51, with therapeutic potential to restore muscle Dp427 expression and motor functions (Aoki et al., 2010; Aupy et al., 2020). Therefore, it is important to determine the behavioral profile and neurobiological bases of central deficits of mdx52 mice to identify the relevant outcome measures for using this model in preclinical studies.

The absence of gross macroscopic changes was confirmed by comparing the lengths of the main cerebral arteries forming the Willis circle (Fig. 1B), as estimated by angiography [genotype effect, F (1,16)=0.56, P>0.45; genotypedistance interaction, F (2,32)=0.86, P>0.42]. Moreover, T2 maps analyses (Fig. 1C) were undertaken in four main regions: we discriminated the primary sensory cortex and the piriform cortex, a prominent cortical area of the rodent brain, important as a main recipient of olfactory inputs and for its widespread projections to forebrain structures, such as the amygdala and the thalamus. We also analyzed the hippocampus, a major structure involved in cognitive functions, and the thalamus, which has extensive connections to the cerebral cortex and midbrain, and plays a major role in relaying motor and sensory signals between subcortical, cerebellar and cortical areas. The T2 maps analyses did not reveal any overall effect of genotype [F (1,18)=0.78, P>0.38] in the four selected regions [genotyperegion interaction: F (3,54)=1.15, P>0.33], suggesting an absence of major alterations of white-matter tissue microstructure.

In this study, we further investigated amygdala-dependent behaviors and learning performance in mdx and mdx52 mice. In the original mdx mouse, the presence of anxiety-related responses has been reported, yet the variability among laboratories and the lack of phenotype in the elevated plus-maze test suggested that the changes in anxiety are borderline in mdx mice (Manning et al., 2014; Sekiguchi et al., 2009; Vaillend and Chaussenot, 2017). Our present results confirmed this conclusion for mdx mice, but further revealed that mdx52 mice display clearer and significant behavioral changes in all behavioral parameters reflecting anxiety during exploration of the light/dark box, elevated plus maze and open field. It has been reported that muscle wasting may be more severe when mutations affecting expression of muscle Dp427 are expressed in a C57BL/6 background compared with the original C57BL/10 background (Beastrom et al., 2011). Although this may potentially constitute a confounding factor in behavioral analyses, we previously showed in mdx mice that reactivity to stress influences locomotor activity, which is otherwise unaltered in unstressed animals (Vaillend and Chaussenot, 2017). In the present study, measures of anxiety were robust in tests with low motor demand, and we normalized anxiety-related parameters to the locomotor activity of an individual to further minimize putative influence of motor factors in our analyses. Besides, the genetic background may also influence brain and behavioral functions (Mortazavi et al., 2021 preprint), which cannot be ruled out without direct comparisons with controls in the same background. Some behavioral parameters were comparable between control mice of the two genetic backgrounds but some others were statistically different, and we therefore preferred to rigorously compare the mutant mice to their respective littermate controls. The significant differences between mdx52 mice and their littermate controls compared to the non-significant differences between mdx mice and their littermate controls suggest that emotional reactivity may be more affected in mdx52 than in mdx mice. This is also in line with the significant deficit shown by mdx52 mice in the elevated plus maze, which was not observed in mdx mice in the present study, as well as in previous reports (Sekiguchi et al., 2009; Vaillend and Chaussenot, 2017). So far, in the present study, we cannot claim a definitive conclusion regarding the severity of the behavioral changes potentially linked to the mutation profile, yet our data show that there are important emotional disturbances in mdx52 mice that represent robust outcome measures that can be used to evaluate treatment efficacy in future preclinical studies.

Fear conditioning performance was replicated several times by our group in identical experimental conditions in mdx mice: the phenotype of this model lacking only Dp427 was consistently characterized by delayed acquisition and retention of the task, but mdx mice could finally perform in a comparable manner to their wild-type littermates after repetition of stimulus presentation (Chaussenot et al., 2015; Vaillend and Chaussenot, 2017). In marked contrast, we found here that mdx52 mice were more severely impaired as they failed to improve their learning performance to reach wild-type performance level and consistently displayed reduced fear responses when auditory CS were presented. However, mdx52 mice showed similar levels of fear responses as wild-type mice following electric shock delivery during the intervals between CS presentations, indicating that the difference cannot be simply explained by a reduced sensitivity to electric shocks or different expression of fear responses. ff782bc1db