Developmental anatomy of <i>reeler</i> mutant mouse

Katsuyama, Yu; Terashima, Toshio

doi:10.1111/j.1440-169x.2009.01102.x

Cited by 54 publications

(52 citation statements)

References 146 publications

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“…However, the type of death striking these two types of neurons is often controversial, particularly regarding PNs in Lurcher (Table 4). Altogether the pattern of neuronal degeneration in Lurcher indicates that multiple Falconer (1951), Mariani et al (1977), Mikoshiba et al (1980), Heckroth et al (1989), Yuasa et al (1993), D'Arcangelo et al (1995 and Katsuyama and Terashima (2009) …”

Section: Comparative Analysis Of Cell Death/neurodegeneration In Cerementioning

confidence: 97%

Cell death and neurodegeneration in the postnatal development of cerebellar vermis in normal and Reeler mice

Castagna

Merighi

2016

Annals of Anatomy - Anatomischer Anzeiger

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Section: Comparative Analysis Of Cell Death/neurodegeneration In Cerementioning

confidence: 97%

Cell death and neurodegeneration in the postnatal development of cerebellar vermis in normal and Reeler mice

Castagna

Merighi

2016

Annals of Anatomy - Anatomischer Anzeiger

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“…Furthermore, neurons appear to retain their correct properties despite their ectopic positions. Molecular markers typically expressed in a layer-specific fashion are still expressed by displaced neurons (Katsuyama and Terashima, 2009; Boyle et al, 2011; Wagener et al, 2016), suggesting that their molecular identity is not compromised by the lack of lamination. The morphology of defined neuronal types has been investigated in some detail and is relatively unchanged (Guy et al, 2016), although some excitatory types see a reduction in the number of dendritic spines (Niu et al, 2008), and some inhibitory types have longer dendrites with more branches (Yabut et al, 2007).…”

Section: The Reeler Neocortex As a Model Systemmentioning

confidence: 99%

The Functioning of a Cortex without Layers

Guy

Staiger

2017

Front. Neuroanat.

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A major hallmark of cortical organization is the existence of a variable number of layers, i.e., sheets of neurons stacked on top of each other, in which neurons have certain commonalities. However, even for the neocortex, variable numbers of layers have been described and it is just a convention to distinguish six layers from each other. Whether cortical layers are a structural epiphenomenon caused by developmental dynamics or represent a functionally important modularization of cortical computation is still unknown. Here we present our insights from the reeler mutant mouse, a model for a developmental, “molecular lesion”-induced loss of cortical layering that could serve as ground truth of what an intact layering adds to the cortex in terms of functionality. We could demonstrate that the reeler neocortex shows no inversion of cortical layers but rather a severe disorganization that in the primary somatosensory cortex leads to the complete loss of layers. Nevertheless, the somatosensory system is well organized. When exploring an enriched environment with specific sets of whiskers, activity-dependent gene expression takes place in the corresponding modules. Precise whisker stimuli lead to the functional activation of somatotopically organized barrel columns as visualized by intrinsic signal optical imaging. Similar results were obtained in the reeler visual system. When analyzing pathways that could be responsible for preservation of tactile perception, lemniscal thalamic projections were found to be largely intact, despite the smearing of target neurons across the cortical mantle. However, with optogenetic experiments we found evidence for a mild dispersion of thalamic synapse targeting on layer IV-spiny stellate cells, together with a general weakening in thalamocortical input strength. This weakening of thalamic inputs was compensated by intracortical mechanisms involving increased recurrent excitation and/or reduced feedforward inhibition. In conclusion, a layer loss so far only led to the detection of subtle defects in sensory processing by reeler mice. This argues in favor of a view in which cortical layers are not an essential component for basic perception and cognition. A view also supported by recent studies in birds, which can have remarkable cognitive capacities despite the lack of a neocortex with multiple cortical layers. In conclusion, we suggest that future studies directed toward understanding cortical functions should rather focus on circuits specified by functional cell type composition than mere laminar location.

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“…The changes in the growth and remodeling of Purkinje cell dendrites are an evident proof of brain plasticity as shown during postnatal histogenesis after X-ray irradiation or treatment with cytotoxic substances (Ferguson, 1996;Avella et al, 2006;Li et al, 2006) or in mutant mice (for a review see Katsuyama and Terashima, 2009). …”

Section: Defects Of Cerebellum Fissuresmentioning

confidence: 99%

Postnatal Development of the Central Nervous System: Anomalies in the Formation of Cerebellum Fissures

Cerri¹,

Piccolini²,

Bernocchi³

2010

The Anatomical Record

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A natural defect in rat cerebellum postnatal development has been found in the fissura prima, consisting in various complex configurations of the cerebellar layers. We investigated the genesis of fissure malformations through immunoreactions for PCNA, GFAP, GABAA a6, and calbindin to label proliferating cells of the external granular layer (egl), radial glial fibers, mature granule cells, and Purkinje cells, respectively. Results on critical stages of rat postnatal development provided interesting evidences on how the malformation develops in fissures prima and secunda. Early (postnatal day 10) at the site of malformation, the Bergmann radial glia was often retracted and showed distortions and irregular running. The interruption of GFAP-positive radial glial fibers could fit in with the presence of clusters of PCNA-unlabeled cells in the sites of fusion of the egl; the clusters of cells are granule cells since their soma is labeled by GABAA a6. Moreover, an altered migration of granule cell precursors to the internal granular layer was evident which, in turn, affected Purkinje cell differentiation and the growth of their dendrites. In summary, the changed relationship among glial fiber morphology, granule cell migration, and Purkinje cell differentiation suggests how the Bergmann glial fibers have a basic role in the foliation process, being the driving physical force in directing migration of the granule cells at the base of fissure. Anat Rec, 293:492-501, 2010. V V C 2010 Wiley-Liss, Inc.

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Developmental anatomy of reeler mutant mouse

Cited by 54 publications

References 146 publications

Cell death and neurodegeneration in the postnatal development of cerebellar vermis in normal and Reeler mice

Cell death and neurodegeneration in the postnatal development of cerebellar vermis in normal and Reeler mice

The Functioning of a Cortex without Layers

Postnatal Development of the Central Nervous System: Anomalies in the Formation of Cerebellum Fissures

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