Cortical Architecture, Midline Guidance, and Tractography of 3D White Matter Tracts

Morcom, Laura; Edwards, Timothy J.; Richards, Linda J.

doi:10.1016/b978-0-12-801393-9.00014-1

Cited by 12 publications

(9 citation statements)

References 215 publications

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“…In search of the etiology of this defect, we assessed the potential structures that could be affected and, at the same time, take part in the development of the CC. Normal CC development depends on guidepost cells that guide the pioneer axons toward the midline, reviewed by Morcom et al (2016), known as the indusium griseum (IG), which is composed by neurons and glia and a lateral mixed neuronal/glial population, known as the glial sling (Silver et al, 1982; Shu and Richards, 2001; Shu et al, 2003). Interestingly, the neurons of the IG are found in part in the Emx1 + domain (Niquille et al, 2009).…”

Section: Resultsmentioning

confidence: 99%

Ablation of CNTN2+ Pyramidal Neurons During Development Results in Defects in Neocortical Size and Axonal Tract Formation

Kastriti

Stratigi

Mariatos

et al. 2019

Front. Cell. Neurosci.

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Corticothalamic axons express Contactin-2 (CNTN2/TAG-1), a neuronal recognition molecule of the immunoglobulin superfamily involved in neurogenesis, neurite outgrowth, and fasciculation. TAG-1, which is expressed transiently by cortical pyramidal neurons during embryonic development, has been shown to be fundamental for axonal recognition, cellular migration, and neuronal proliferation in the developing cortex. Although Tag-1−/− mice do not exhibit any obvious defects in the corticofugal system, the role of TAG-1+ neurons during the development of the cortex remains elusive. We have generated a mouse model expressing EGFP under the Tag-1 promoter and encompassing the coding sequence of Diptheria Toxin subunit A (DTA) under quiescence with no effect on the expression of endogenous Tag-1. We show that while the line recapitulates the expression pattern of the molecule, it highlights an extended expression in the forebrain, including multiple axonal tracts and neuronal populations, both spatially and temporally. Crossing these mice to the Emx1-Cre strain, we ablated the vast majority of TAG-1+ cortical neurons. Among the observed defects were a significantly smaller cortex, a reduction of corticothalamic axons as well as callosal and commissural defects. Such defects are common in neurodevelopmental disorders, thus this mouse could serve as a useful model to study physiological and pathophysiological cortical development.

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Section: Resultsmentioning

confidence: 99%

Ablation of CNTN2+ Pyramidal Neurons During Development Results in Defects in Neocortical Size and Axonal Tract Formation

Kastriti

Stratigi

Mariatos

et al. 2019

Front. Cell. Neurosci.

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“…Although the exact function of hippocampal rudiments structures is not well known, they are believed to play an important role in axonal guidance across the midline during development of brain commissures and interhemispheric connections. 34 The damage of these structures during HI may lead to a spectrum of neurodevelopmental conditions. 35 Expression of ARG-2 in hippocampal rudiments suggests important roles for ARG-2 in mediating at least some of these functions.…”

Section: Discussionmentioning

confidence: 99%

Changes in arginase isoforms in a murine model of neonatal brain hypoxia–ischemia

et al. 2020

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BACKGROUND: Arginases (ARG isoforms, ARG-1/ARG-2) are key regulatory enzymes of inflammation and tissue repair; however, their role after neonatal brain hypoxia (H) and hypoxia-ischemia (HI) remains unknown. METHODS: C57BL/6 mice subjected to the Vannucci procedure on postnatal day (P9) were sacrificed at different timepoints. The degree of brain damage was assessed histologically. ARG spatiotemporal localization was determined via immunohistochemistry. ARG expression was measured by Western blot and activity spectrophotometrically. RESULTS: ARG isoform expression increased during neurodevelopment (P9-P17) in the cortex and hippocampus. This was suppressed with H and HI only in the hippocampus. In the cortex, both isoforms increased with H alone and only ARG-2 increased with HI at 3 days. ARG activity during neurodevelopment remained unchanged, but increased at 1 day with H and not HI. ARG-1 localized with microglia at the injury site as early as 4 h after injury, while ARG-2 localized with neurons. CONCLUSIONS: ARG isoform expression increases with age from P9 to P17, but is suppressed by injury specifically in the hippocampus and not in the cortex. Both levels and activity of ARG isoforms increase with H, while ARG-1 immunolabelling is upregulated in the HI cortex. Evidently, ARG isoforms in the brain differ in spatiotemporal localization, expression, and activity during neurodevelopment and after injury.

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“…CC formation is dependent on a prior sequence of developmental processes: cellular proliferation, migration, axonal elongation, guidance and targeting (Donahoo and Richards, 2009;Edwards et al, 2014;Morcom et al, 2015). Callosal axons derived from cells within the cingulate and neocortices elongate and cross the telencephalic midline in a region of the septum termed the commissural plate (Moldrich et al, 2010;Rakic and Yakovlev, 1968).…”

Section: Introductionmentioning

confidence: 99%

DRAXIN regulates interhemispheric fissure remodelling to influence the extent of corpus callosum formation

Morcom

Edwards

Rider

et al. 2020

Preprint

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Corpus callosum dysgenesis (CCD) is a congenital disorder that incorporates either partial or complete absence of the largest cerebral commissure. Remodelling of the interhemispheric fissure (IHF) provides a substrate for callosal axons to cross between hemispheres, and its failure is the main cause of complete CCD. However, it is unclear whether defects in this process could give rise to the heterogeneity of expressivity and phenotypes seen in human cases of CCD. We identify incomplete IHF remodelling as the key structural correlate for the range of callosal abnormalities in inbred and outcrossed BTBR mouse strains, as well as in humans with partial CCD. We identify an eight base pair deletion in Draxin and misregulated astroglial and leptomeningeal proliferation as genetic and cellular factors for variable IHF remodelling and CCD in BTBR acallosal strains. These findings support a model where genetic events determine corpus callosum structure by influencing leptomeningeal-astroglial interactions at the IHF.

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Cortical Architecture, Midline Guidance, and Tractography of 3D White Matter Tracts

Cited by 12 publications

References 215 publications

Ablation of CNTN2+ Pyramidal Neurons During Development Results in Defects in Neocortical Size and Axonal Tract Formation

Ablation of CNTN2+ Pyramidal Neurons During Development Results in Defects in Neocortical Size and Axonal Tract Formation

Changes in arginase isoforms in a murine model of neonatal brain hypoxia–ischemia

DRAXIN regulates interhemispheric fissure remodelling to influence the extent of corpus callosum formation

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