Predominant Localization of the LIS Family of Gene Products to Cajal-Retzius Cells and Ventricular Neuroepithelium in the Developing Human Cortex

Clark, Gary D.; Mizuguchi, Masashi; Antalffy, Barbara; Barnes, James E.; Armstrong, Dawna

doi:10.1097/00005072-199709000-00009

Cited by 55 publications

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“…This was not the case, because we observed a differential, highly selective elimination of a subpopulation of C-R cells. The identification of several subpopulations of layer I cells with selective persistence in primates may help in elucidating their possible role in congenital malformations of the human cerebral cortex such as lissencephaly (Clark et al, 1997;Hong et al, 2000).…”

Section: Function and Fatementioning

confidence: 99%

“…Although these cells have continued to fascinate investigators, a recent discovery that they produce reelin, a glycoprotein essential for orderly neuronal cell migration and ingrowth of afferents into the cerebral cortex, has augmented this attention (D'Arcangelo et al, 1995(D'Arcangelo et al, , 1997Ogawa et al, 1995;Del Rio et al, 1997;Nakajima et al, 1997;Curran and D'Arcangelo, 1998). It was also suggested that C-R cells may be involved in developmental disorders of the cerebral cortex in humans (Rakic and Caviness, 1995;Clark et al, 1997;Impagnatiello et al, 1998;Hong et al, 2000).…”

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confidence: 99%

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Development of Layer I Neurons in the Primate Cerebral Cortex

2001

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Section: Function and Fatementioning

confidence: 99%

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confidence: 99%

Development of Layer I Neurons in the Primate Cerebral Cortex

2001

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“…Cajal-Retzius cells also have an important role during normal cortical development. Their impairment is related to developmental disorders of the human cerebral cortex with disturbed neural migration, resulting in lissencephaly and mental retardation (Rakic and Caviness, 1995;Clark et al, 1997;Hong et al, 2000). Additional roles for Cajal-Retzius cells, such as in schizophrenia (Impagnatiello et al, 1998), or in repair of brain lesions (Super et al, 1997) have been suggested.…”

Section: Introductionmentioning

confidence: 99%

Emerging Complexity of Layer I in Human Cerebral Cortex

Rakić

Zečević²

2003

Cerebral Cortex

142

133

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In this study we examine possible origins and migratory routes of human cortical neurons, with special emphasis on the preplate and layer I. In embryonic stages, two main cell types, Cajal-Retzius cells, and cells labeled with interneuron markers (calretinin, calbindin and GABA), were present in the preplate layer. In addition, a number of preplate GABAergic cells co-expressed either Nkx2.1 or Dlx transcription factors, findings consistent with their origin in the ganglionic eminence and subsequent tangential migration to the layer I. The orientation of the leading process indicates that some of these cells descend to the cortical plate. However, the finding of radially oriented GABAergic, NKX2.1 + and DLX + cells in the cortical ventricular zone, argues that, unlike in rodents, a significant subpopulation of these cells originates in the cortical ventricular zone. In embryonic stages, expression of Reelin in Cajal-Retzius cells as well as Reelin/DLX2 + cells in the embryonic ganglionic eminence and the olfactory region, suggest that these cells in human may have diverse origins. In later fetal stages in human (17-22 gestational weeks) layer I and the newly formed subpial granular layer, contained a population of small interneurons that originated mainly in the lateral ganglionic eminence, since the majority of these cells were double-labeled with DLX/GABA, and rarely with NKX2.1/GABA. Therefore, neurons in the human cortical layer I are heterogeneous, with more complex origin and migratory routes than in rodents. In addition to the ganglionic eminence, both the expended subventricular zone and subpial granular layer, contribute to the neuronal population of the developing layer I and underlining cortical plate.

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“…5,6 This gene encodes the ␤ subunit of brain type platelet-activating factor acetylhydrolase (PAFAH1B1), 7 which is present in abundance in normal brains but is deficient in those of patients with MDS. 8,9 On the other hand, ILS consists of heterogeneous conditions. Approximately 40% of sporadic ILS patients have a deletion of 17p13.3 involving the LIS1 gene.…”

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confidence: 99%

High Expression of Doublecortin and KIAA0369 Protein in Fetal Brain Suggests Their Specific Role in Neuronal Migration

Mizuguchi

Qin

Yamada

et al. 1999

The American Journal of Pathology

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The X-linked subcortical laminar heterotopia and lissencephaly syndrome is a disorder of neuronal migration caused by a mutation in XLIS, a recently cloned gene on chromosome Xq22.3-q23. The predicted protein product for XLIS, doublecortin (DC), shows high homology to a putative calcium calmodulin-dependent kinase , KIAA0369 protein (KI). Here we identified DC and KI in the brains of human and rat fetuses by immunochemical and immunohistochemical means. In this study , Western blotting demonstrated that both DC and KI are specific to the nervous system and are abundant during the fetal period , around 20 gestational weeks in humans and embryonic days 17 to 20 in rats. Immunostaining of the developing neocortex disclosed localization of DC and KI immunoreactivities in neuronal cell bodies and processes in the zones of ongoing neuronal migration. Although KI showed a somewhat wider distribution than DC , the temporal and spatial patterns of their expression were similar. These results suggest that DC and KI participate in a common signaling pathway regulating neuronal migration. (Am J Pathol 1999, 155:1713-1721)

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Predominant Localization of the LIS Family of Gene Products to Cajal-Retzius Cells and Ventricular Neuroepithelium in the Developing Human Cortex

Cited by 55 publications

References 0 publications

Development of Layer I Neurons in the Primate Cerebral Cortex

Development of Layer I Neurons in the Primate Cerebral Cortex

Emerging Complexity of Layer I in Human Cerebral Cortex

High Expression of Doublecortin and KIAA0369 Protein in Fetal Brain Suggests Their Specific Role in Neuronal Migration

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