A segmentation protocol and MRI atlas of the C57BL/6J mouse neocortex

Ullmann, Jeremy F.P.; Watson, Charles; Janke, Andrew L.; Kurniawan, Nyoman D.; Reutens, David C.

doi:10.1016/j.neuroimage.2013.04.008

Cited by 203 publications

(155 citation statements)

References 36 publications

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“…Regional volumes were determined using a pre‐existing classified MRI atlas encompassing 159 different structures throughout the brain (Dorr, Lerch, Spring, Kabani, & Henkelman, 2008; Steadman et al, 2014; Ullmann, Watson, Janke, Kurniawan, & Reutens, 2013). Statistical analyses were applied comparing the absolute and relative volume of these 159 different regions and on a voxel‐wise basis in the brains of control and Chd7 gt/+ mice.…”

Section: Methodsmentioning

confidence: 99%

Distinct cerebellar foliation anomalies in a CHD7 haploinsufficient mouse model of CHARGE syndrome

Whittaker

Kasah

Donovan

et al. 2017

American J of Med Genetics Pt C

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Mutations in the gene encoding the ATP dependent chromatin‐remodeling factor, CHD7 are the major cause of CHARGE (Coloboma, Heart defects, Atresia of the choanae, Retarded growth and development, Genital‐urinary anomalies, and Ear defects) syndrome. Neurodevelopmental defects and a range of neurological signs have been identified in individuals with CHARGE syndrome, including developmental delay, lack of coordination, intellectual disability, and autistic traits. We previously identified cerebellar vermis hypoplasia and abnormal cerebellar foliation in individuals with CHARGE syndrome. Here, we report mild cerebellar hypoplasia and distinct cerebellar foliation anomalies in a Chd7 haploinsufficient mouse model. We describe specific alterations in the precise spatio‐temporal sequence of fissure formation during perinatal cerebellar development responsible for these foliation anomalies. The altered cerebellar foliation pattern in Chd7 haploinsufficient mice show some similarities to those reported in mice with altered Engrailed, Fgf8 or Zic1 gene expression and we propose that mutations or polymorphisms in these genes may modify the cerebellar phenotype in CHARGE syndrome. Our findings in a mouse model of CHARGE syndrome indicate that a careful analysis of cerebellar foliation may be warranted in patients with CHARGE syndrome, particularly in patients with cerebellar hypoplasia and developmental delay.

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Section: Methodsmentioning

confidence: 99%

Distinct cerebellar foliation anomalies in a CHD7 haploinsufficient mouse model of CHARGE syndrome

Whittaker

Kasah

Donovan

et al. 2017

American J of Med Genetics Pt C

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“…The previous papers in the series dealt with the hippocampus (Richards et al, 2011), the cerebellum (Ullmann et al, 2012), the basal ganglia (Ullmann et al, 2014), and the cerebral cortex (Ullmann et al, 2013). The present paper offers a detailed description of the major parts of the mouse diencephalon in high-resolution MR images.…”

Section: Discussionmentioning

confidence: 93%

“…The FSL atlas package used by our consortium includes labels for the segmentation of the mouse diencephalon, as well as the previous AMBMC atlases including the basal ganglia (Ullmann et al, 2014), cerebellum (Ullmann et al, 2012), cerebral cortex (Ullmann et al, 2013), and hippocampus (Richards et al, 2011). Additionally, a symmetric average mouse brain MRI model is included in the package that should be used for image registrations (Janke and Ullmann, 2015).…”

Section: The Pretectal Nuclei (Prosomere 1)mentioning

confidence: 99%

“…Recently, there has been an increase in the number of studies investigating the mouse thalamus using functional, structural, and diffusion-weighted imaging (DWI) techniques to examine neurological disorders and map brain connectivity (Ferris et al, 2014;Keifer et al, 2015;Maheswaran et al, 2009;Malkova et al, 2014;Nessler et al, 2007;Richards et al, 2014;Shu et al, 2013). However, these studies have relied upon manual segmentation of the diencephalon or have used atlases that identify only a limited number of diencephalic structures (Dorr et al, 2008;Kovacevic et al, 2005;Ma et al, 2005;MacKenzieGraham et al, 2004;Ullmann et al, 2012;Ullmann et al, 2014;Ullmann et al, 2013). In response to this limitation, we have endeavoured to create a comprehensive probabilistic atlas of the C57BL/6J mouse diencephalon.…”

Section: Introductionmentioning

confidence: 99%

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An ontologically consistent MRI-based atlas of the mouse diencephalon

et al. 2017

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“…Six ROIs were selected based on anatomical relevance, the cingulate cortex, primary somatosensory cortex (barrel field), insular cortex, caudate-putamen, and hippocampus were based on the AMBMC atlas (Richards et al, 2011;Ullmann et al, 2013;Ullmann et al, 2014) and the thalamus was based on . Data extracted from left and right ROIs were combined for analysis (Figure 3-1).…”

Section: Roi Analysismentioning

confidence: 99%

Functional network study on the wild type and DISC1 transgenic mice

Wu¹

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Major mental disorders such as schizophrenia (SZ), bipolar disorder and major depression create a heavy social burden and remain poorly treated. Recent reports examining the genetic and molecular structure of brain disorders discovered the gene Disrupted-in-Schizophrenia 1 (DISC1) to be significantly associated with these disorders and plays a substantial role in influencing a range of shared endophenotypes underlying these disorders. This has led to a powerful gateway to explore the underlying pathology and to achieve better diagnosis and treatments of major mental diseases. Characterising the phenotypes of DISC1 in brain functions would provide valuable insights into the mechanism of how this gene influences the brain.Resting-state fMRI (rs-fMRI) is a powerful technique being applied to more than 30 different kinds of brain disorders and different species. Findings from rs-fMRI studies on humans provide ample evidence of abnormal functional patterns in patients with mental illnesses. Specifically, altered functional connectivity (FC) and network topologies are proposed to be plausible imaging endophenotypes of psychotic disorders. However, little is known about the direct effects of gene dysfunction, such as DISC1 mutations, on restingstate brain activations. One aim of this thesis is to investigate the impacts of DISC1 on variations of resting-state functional networks (RSNs) in anaesthetized mouse brains using DISC1 transgenic mice and rs-fMRI.Before characterizing disease phenotypes in mouse models, it is necessary to understand how the mouse brain functions in normal states. Anaesthesia is currently an integrated part of most mouse rs-fMRI experiment. However, it influences blood-oxygenation-leveldependent (BOLD) fMRI signals via modulation of neurovascular coupling and brain metabolism, and therefore alters FC and topologies of RSNs. Investigating FC and its changes associated with genes therefore initially requires an understanding of the anaesthetics. Furthermore, various anaesthetic protocols are adopted by different labs leading to difficulties in result comparisons. The brain is a complex and hierarchical system, whereby its RSN architecture can be characterised from mutiple perspectives at regional or global levels. Previous mouse rs-fMRI studies have focused on long-distance FC, however, given the non-uniform influence of anaesthesia on the brain, mapping functional activations across scales in mice under different anaesthetics remain sparsely explored. Establishing this relationahsip would provide a reliable reference to study mouse brain functions in abnormal states and facilitate comparisons across laboratories. | P a g eIn the first aim of this thesis, I investigated the local connectivity in wide type (WT) mice under six commonly used anaesthetic regimens. I identified that the regional connectivity altered across the brain as a function of the expression density of receptors relative to specific agents. In addition, the depth of anaesthesia influences local synchronization.In the seco...

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A segmentation protocol and MRI atlas of the C57BL/6J mouse neocortex

Cited by 203 publications

References 36 publications

Distinct cerebellar foliation anomalies in a CHD7 haploinsufficient mouse model of CHARGE syndrome

Distinct cerebellar foliation anomalies in a CHD7 haploinsufficient mouse model of CHARGE syndrome

An ontologically consistent MRI-based atlas of the mouse diencephalon

Functional network study on the wild type and DISC1 transgenic mice

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