The development of the mammalian nervous system I. Malformations of the brain, especially the cerebral cortex, induced in rats by radiation II. Some mechanisms of the malformations of the cortex

Hicks, Samuel P.; D’Amato, Constance J.; Lowe, Mary Jane

doi:10.1002/cne.901130306

Cited by 166 publications

(46 citation statements)

References 4 publications

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“…Rosette formation and the formation of rosette-like structures under various conditions werc considered t o be a fundamental property of developing nervous tissues of vertebrate embryos and fetuses (WATTERSON, 1965). In the case of neural retina, it has been shown that the rosettes which were formcd after X-ray irradiation had well-oriented walls corresponding t o the iiormal structure of retina (HICKS, D'AMATO and LOWES, 1959). In the present study, at 4 days after grafting, the differentiated receptor layer was formed inside the rosettes (see Fig.…”

Section: Discussionsupporting

confidence: 54%

A Complete Reconstruction of the Neural Retina of Chick Embryo Grafted Onto the Chorio-Allantoic Membrane

Fujisawa

1971

Dev Growth Differ

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When dissociated neural retinal cells of 6-to 10-day-old chick embryos were grafted as a pellet onto the chorio-allantoic membrane and allowed to develop, complete retinal structures were reconstructed. Especially when the retinal cells of 6-day-old embryos were used, well orientated retinal structures, which possesed three nuclear layers and two plexiform layers, were formed. The fundamental steps in this complete reconstruction were as follows; rosette formation, formation of a fibrillar lumen, differentiation of receptor and ganglion cells, fusion of the fibrillar lumen, fusion of the receptor lumen and finally the formation of a three-layered neural retina. Reconstruction by the retinal cells of older embryos was less complete. This stagedependent difference in the capacity for reconstruction was due to a difference in the ability to form well developed rosettes at an early phase of the process of reconstruction.

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Section: Discussionsupporting

confidence: 54%

A Complete Reconstruction of the Neural Retina of Chick Embryo Grafted Onto the Chorio-Allantoic Membrane

Fujisawa

1971

Dev Growth Differ

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“…Other studies investigating animal models of cortical dysplasia with experimentally induced disruption of cortical development also suggest a causal link between cortical malformations and seizure activity (Chevassus-au-Louis et al, 1999;Walsh, 1999;Fleck et al, 2000;Chen et al, 2000). Such animal models include migrational malformations induced by freezing (Dvorak and Feit, 1977;Dvorak et al, 1978;Rosen et al, 1992Rosen et al, , 1996Jacobs et al, 1996, Hablitz andDeFazio, 1998), x-irradiation (Roper et al, 1995(Roper et al, , 1997Hicks et al, 1959), and chemical treatment (e.g., methylazoxymethanol : Singh, 1977;Cattaneo et al, 1995;De Feo et al, 1995;Baraban and Schwartzkroin, 1996;Germano and Sperber, 1997;Chevassus-au-Louis et al, 1998Baraban et al, 2000). Animals with abnormalities paralleling human genetic neuronal migration disorders also show enhanced seizure-sensitivity: e.g., type 1 lissencephaly (Lis1 mutant) (Reiner et al, 1993;Hirotsune et al, 1998;Fleck et al, 2000), and band heterotopia (tish mutant) (Lee et al, 1997).…”

Section: Discussionmentioning

confidence: 99%

Abnormal Morphological and Functional Organization of the Hippocampus in a p35 Mutant Model of Cortical Dysplasia Associated with Spontaneous Seizures

Wenzel¹,

Robbins²,

Tsai

et al. 2001

J. Neurosci.

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Cortical dysplasia is a major cause of intractable epilepsy in children. However, the precise mechanisms linking cortical malformations to epileptogenesis remain elusive. The neuronalspecific activator of cyclin-dependent kinase 5, p35, has been recognized as a key factor in proper neuronal migration in the neocortex. Deletion of p35 leads to severe neocortical lamination defects associated with sporadic lethality and seizures. Here we demonstrate that p35-deficient mice also exhibit dysplasia/ heterotopia of principal neurons in the hippocampal formation, as well as spontaneous behavioral and electrographic seizures. Morphological analyses using immunocytochemistry, electron microscopy, and intracellular labeling reveal a high degree of abnormality in dentate granule cells, including heterotopic localization of granule cells in the molecular layer and hilus, aberrant dendritic orientation, occurrence of basal dendrites, and abnormal axon origination sites. Dentate granule cells of p35-deficient mice also demonstrate aberrant mossy fiber sprouting. Field potential laminar analysis through the dentate molecular layer reflects the dispersion of granule cells and the structural reorganization of this region. Similar patterns of cortical disorganization have been linked to epileptogenesis in animal models of chronic seizures and in human temporal lobe epilepsy. The p35-deficient mouse may therefore offer an experimental system in which we can dissect out the key morphological features that are causally related to epileptogenesis.

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“…Both treatments usually occur around embryonic days 14-1 6 in rats. MAM (47) and irradiation (48) are basically antimitotic treatments that selectively kill dividing cells in the proliferative epithelium. In addition, these treatments can cause indirect lesions of radial glial fibers, resulting in neuronal migration disorders (49,50).…”

Section: In Utero Insultsmentioning

confidence: 99%

Cortical Malformations and Epilepsy: New Insights from Animal Models

et al. 1999

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Summary:In the last decade, the recognition of the high frequency of cortical malformations among patients with epilepsy especially children, has led to a renewed interest in the study of the pathophysiology of cortical development. This field has also been spurred by the recent development of several experimental genetic and non-genetic, primarily rodent, models of cortical malformations. Epileptiform activity in these animals can appear as spontaneous seizure activity in vivo, in vitro hyperexcitability, or reduced seizure susceptibility in vitro and in vivo. In the neonatal freeze lesion model, that mimics human microgyria, hyperexcitability is caused by a reorganization of the network in the borders of the malformation. In the prenatal methylazoxymethanol model, that causes a diffuse cortical malformation, hyperexcitability is associated with alteration of firing properties of discrete neuronal subpopulations together with the formation of bridges between normally unconnected structures. In agreement with clinical evidence, these expenmental data suggest that cortical malformations can both form epileptogenic foci and alter brain development in a manner that causes a diffuse hyperexcitability of the cortical network. Key Words: Neocortex-Hippocampus-Development-Neuronal migration-Methylazoxymethanol.As early as the end of the nineteenth century, neuropathologists began to report an association between cortical malformations and epilepsy (1-3). Until recently, however, clinical and experimental research yielded few insights into the pathophysiology of this distinct class of epilepsies. In fact, the last decade has seen three major scientific advances that have directly contributed to the "rediscovery" and renewed interest in examining the cause of epilepsy in patients with cortical malformations: mation and epilepsy. Moreover, neuropathologic analysis of resected tissue has frequently demonstrated the presence of more subtle malformations that were not identified in vivo. 3. Recent progress in human molecular genetics has allowed the identification of several genes whose mutations lead to both malformations and epilepsy. In parallel, several genetic and nongenetic rodent models of cortical malformations were shown to be associated with either spontaneous seizures or hyperexcitability .Our goal is to review the contributions of these animal models to our understanding of the pathophysiology of cortical malformations and to discuss their possible link with epilepsy. CORTICAL MALFORMATIONS IN HUMANSHuman cortical malformations have been the subject of several reviews (4-8) and the histology of the major types of cortical malformations encountered is fairly well established (see Fig. 1). In addition, classification of cortical malformations (based on neuropathology, radiology, etiology, or a combination of these elements) has 811

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The development of the mammalian nervous system I. Malformations of the brain, especially the cerebral cortex, induced in rats by radiation II. Some mechanisms of the malformations of the cortex

Cited by 166 publications

References 4 publications

A Complete Reconstruction of the Neural Retina of Chick Embryo Grafted Onto the Chorio-Allantoic Membrane

A Complete Reconstruction of the Neural Retina of Chick Embryo Grafted Onto the Chorio-Allantoic Membrane

Abnormal Morphological and Functional Organization of the Hippocampus in a p35 Mutant Model of Cortical Dysplasia Associated with Spontaneous Seizures

Cortical Malformations and Epilepsy: New Insights from Animal Models

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