The origin and migration of cortical neurones: new vistas

Parnavelas, John G.

doi:10.1016/s0166-2236(00)01553-8

Cited by 374 publications

(247 citation statements)

References 49 publications

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“…1 C-F and black bars in E and F). At this stage of development, the cerebral cortex is composed of several layers, including the VZ, SVZ, and the intermediate zone (IZ), through which neurons and glial cells migrate, as well as the CP (28). In the developing cerebral cortex of Frs2␣ 2F/2F mice, the thickness of the CP was less than half the thickness in WT or Frs2␣ 2F/ϩ mice in all regions of the cerebral cortex ( Fig.…”

Section: Frs2␣ 2f/2f Mutant Mice Exhibit a Profound Defect In Corticomentioning

confidence: 99%

Essential role of Shp2-binding sites on FRS2α for corticogenesis and for FGF2-dependent proliferation of neural progenitor cells

Yamamoto

Yoshino

Shimazaki

et al. 2005

Proc. Natl. Acad. Sci. U.S.A.

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Section: Frs2␣ 2f/2f Mutant Mice Exhibit a Profound Defect In Corticomentioning

confidence: 99%

Essential role of Shp2-binding sites on FRS2α for corticogenesis and for FGF2-dependent proliferation of neural progenitor cells

Yamamoto

Yoshino

Shimazaki

et al. 2005

Proc. Natl. Acad. Sci. U.S.A.

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“…Proliferating neuroepithelial cells in the VZ of the dorsal telencephalon produce the vast majority of cortical projection neurons, although they also give rise to some cells of glial lineage (for review see, Parnavelas, 2000). In the subventricular zone (SVZ), they produce predominantly glial cells, although they also give rise to some supragranular cortical neurons (Takahashi et al, 1995b;Tarabykin et al, 2001;Noctor et al, 2004).…”

Section: Introductionmentioning

confidence: 99%

Insulin-Like Growth Factor-I Accelerates the Cell Cycle by Decreasing G₁Phase Length and Increases Cell Cycle Reentry in the Embryonic Cerebral Cortex

Hodge¹,

D’Ercole²,

O’Kusky³

2004

J. Neurosci.

117

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“…GABA-containing neurons are LacZ negative in these mice. These cortical interneurons most probably maintained their NR1 expression because they derived from the ganglionic eminence of the ventral telencephalon 20 where Emx1 gene is not expressed.…”

mentioning

confidence: 99%

Cortex-restricted disruption of NMDAR1 impairs neuronal patterns in the barrel cortex

Iwasato

Datwani

Wolf

et al. 2000

Nature

469

509

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In the rodent primary somatosensory cortex, the configuration of whiskers and sinus hairs on the snout and of receptor-dense zones on the paws is topographically represented as discrete modules of layer IV granule cells (barrels) and thalamocortical afferent terminals 1,2 . The role of neural activity, particularly activity mediated by NMDARs (N-methyl-D-aspartate receptors), in patterning of the somatosensory cortex has been a subject of debate [3][4][5][6] . We have generated mice in which deletion of the NMDAR1 (NR1) gene is restricted to excitatory cortical neurons, and here we show that sensory periphery-related patterns develop normally in the brainstem and thalamic somatosensory relay stations of these mice. In the somatosensory cortex, thalamocortical afferents corresponding to large whiskers form patterns and display critical period plasticity, but their patterning is not as distinct as that seen in the cortex of normal mice. Other thalamocortical patterns corresponding to sinus hairs and digits are mostly absent. The cellular aggregates known as barrels and barrel boundaries do not develop even at sites where thalamocortical afferents cluster. Our findings indicate that cortical NMDARs are essential for the aggregation of layer IV cells into barrels and for development of the full complement of thalamocortical patterns.The rodent somatosensory system is an excellent model to study molecular mechanisms underlying the establishment of patterned topographic connections between the sensory periphery and the brain. Trigeminal and dorsal column pathways convey a somatosensory map from the periphery to the neocortex by relay stations in the brainstem and the ventrobasal thalamus. At each level, pre-synaptic afferents and their target cells establish a patterned array of modules corresponding to the arrangement of whiskers and sinus hairs on the snout (trigeminal pathway), and receptor-dense zones of the paws (dorsal column pathway) 2,7,8 . These patterns are consolidated during the first postnatal week, and are subject to alterations if the sensory periphery is perturbed by nerve or whisker lesions during a critical period 2,7,8 . Thus, early neural activity might be essential in the development and plasticity of central patterns much like that of the vertebrate visual system 9,10 . Within this context, NMDAR activity has attracted much attention 9,11 . Initial studies using pharmacological blockade of NMDARs in postnatal rat somatosensory cortex did not detect effects on thalamocortical patterning, but revealed functional impairment of thalamocortical connectivity and whisker-specific responsiveness of barrel neurons 4,5 . In contrast, genetic manipulations of NMDARs showed an absence of periphery-related patterns in the somatosensory cortex 6 . This result could not be ascribed to direct effects on the neocortex, however, as it could have been a consequence of impaired patterns at the brainstem level 6,12,13 . To delineate the specific role(s) of cortical NMDARs in patterning, here we disrupted the ...

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The origin and migration of cortical neurones: new vistas

Cited by 374 publications

References 49 publications

Essential role of Shp2-binding sites on FRS2α for corticogenesis and for FGF2-dependent proliferation of neural progenitor cells

Essential role of Shp2-binding sites on FRS2α for corticogenesis and for FGF2-dependent proliferation of neural progenitor cells

Insulin-Like Growth Factor-I Accelerates the Cell Cycle by Decreasing G₁Phase Length and Increases Cell Cycle Reentry in the Embryonic Cerebral Cortex

Cortex-restricted disruption of NMDAR1 impairs neuronal patterns in the barrel cortex

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The origin and migration of cortical neurones: new vistas

Cited by 374 publications

References 49 publications

Essential role of Shp2-binding sites on FRS2α for corticogenesis and for FGF2-dependent proliferation of neural progenitor cells

Essential role of Shp2-binding sites on FRS2α for corticogenesis and for FGF2-dependent proliferation of neural progenitor cells

Insulin-Like Growth Factor-I Accelerates the Cell Cycle by Decreasing G1Phase Length and Increases Cell Cycle Reentry in the Embryonic Cerebral Cortex

Cortex-restricted disruption of NMDAR1 impairs neuronal patterns in the barrel cortex

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Insulin-Like Growth Factor-I Accelerates the Cell Cycle by Decreasing G₁Phase Length and Increases Cell Cycle Reentry in the Embryonic Cerebral Cortex