Reelin is essential for neuronal migration but not for radial glial elongation in neonatal ferret cortex

2008 ◽  
Vol 68 (5) ◽  
pp. 590-604 ◽  
Author(s):  
Alisa Schaefer ◽  
Sylvie Poluch ◽  
Sharon Juliano
Keyword(s):  
Neuronal Migration ◽  
Radial Glial

scholarly journals Crucial Roles of the Arp2/3 Complex during Mammalian Corticogenesis

2015 ◽  
Author(s):  
Pei-Shan Wang ◽  
Fu-Sheng Chou ◽  
Fengli Guo ◽  
Praveen Suraneni ◽  
Sheng Xia ◽  
...  
Keyword(s):  
Cell Fate ◽  
Membrane Trafficking ◽  
Neuronal Migration ◽  
Neuronal Cell ◽  
Leading Edge ◽  
Radial Glial Cells ◽  
A Cell ◽  
Radial Glial ◽  
Altered Cell ◽  
Actin Nucleator

The polarity and organization of radial glial cells (RGCs), which serve as both stem cells and scaffolds for neuronal migration, are crucial for cortical development. However, the cytoskeletal mechanisms that drive radial glial outgrowth and maintain RGC polarity remain poorly understood. Here, we show that the Arp2/3 complex, the unique actin nucleator that produces branched actin networks, plays essential roles in RGC polarity and morphogenesis. Disruption of the Arp2/3 complex in RGCs retards process outgrowth toward the basal surface and impairs apical polarity and adherens junctions. Whereas the former is correlated with abnormal actin-based leading edge, the latter is consistent with blockage in membrane trafficking. These defects result in altered cell fate, disrupted cortical lamination and abnormal angiogenesis. In addition, we present evidence that the Arp2/3 complex is a cell-autonomous regulator of neuronal migration. Our data suggest that Arp2/3-mediated actin assembly may be particularly important for neuronal cell motility in soft or poorly adhesive matrix environment.

Topical Review: Neuronal Migration in Cortical Development

2004 ◽  
Vol 19 (3) ◽  
pp. 274-279
Author(s):  
Shigeaki Kanatani ◽  
Hidenori Tabata ◽  
Kazunori Nakajima
Keyword(s):  
Neuronal Migration ◽  
Radial Glia ◽  
Asymmetric Cell Division ◽  
Time Lapse ◽  
Radial Glial Cells ◽  
Daughter Cells ◽  
Radial Glial ◽  
Time Lapse Imaging ◽  
Mitotic Behavior

Cortical formation in the developing brain is a highly complicated process involving neuronal production (through symmetric or asymmetric cell division) interaction of radial glia with neuronal migration, and multiple modes of neuronal migration. It has been convincingly demonstrated by numerous studies that radial glial cells are neural stem cells. However, the processes by which neurons arise from radial glia and migrate to their final destinations in vivo are not yet fully understood. Recent studies using time-lapse imaging of neuronal migration are giving investigators an increasingly more detailed understanding of the mitotic behavior of radial glia and the migrating behavior of their daughter cells. In this review, we describe recent progress in elucidating neuronal migration in brain formation and how neuronal migration is disturbed by mutations in genes that control this process. ( J Child Neurol 2005;20:274—279).

scholarly journals Intersectin 1 is a component of the Reelin pathway to regulate neuronal migration and synaptic plasticity in the hippocampus

2017 ◽  
Vol 114 (21) ◽  
pp. 5533-5538 ◽  
Author(s):  
Burkhard Jakob ◽  
Gaga Kochlamazashvili ◽  
Maria Jäpel ◽  
Aziz Gauhar ◽  
Hans H. Bock ◽  
...  
Keyword(s):  
Synaptic Plasticity ◽  
Neuronal Migration ◽  
Pyramidal Neurons ◽  
Neurological Diseases ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Long Term Potentiation ◽  
Downstream Signaling ◽  
Radial Glial ◽  
Reelin Signaling

Brain development and function depend on the directed and coordinated migration of neurons from proliferative zones to their final position. The secreted glycoprotein Reelin is an important factor directing neuronal migration. Loss of Reelin function results in the severe developmental disorder lissencephaly and is associated with neurological diseases in humans. Reelin signals via the lipoprotein receptors very low density lipoprotein receptor (VLDLR) and apolipoprotein E receptor 2 (ApoER2), but the exact mechanism by which these receptors control cellular function is poorly understood. We report that loss of the signaling scaffold intersectin 1 (ITSN1) in mice leads to defective neuronal migration and ablates Reelin stimulation of hippocampal long-term potentiation (LTP). Knockout (KO) mice lacking ITSN1 suffer from dispersion of pyramidal neurons and malformation of the radial glial scaffold, akin to the hippocampal lamination defects observed in VLDLR or ApoER2 mutants. ITSN1 genetically interacts with Reelin receptors, as evidenced by the prominent neuronal migration and radial glial defects in hippocampus and cortex seen in double-KO mice lacking ITSN1 and ApoER2. These defects were similar to, albeit less severe than, those observed in Reelin-deficient or VLDLR/ ApoER2 double-KO mice. Molecularly, ITSN1 associates with the VLDLR and its downstream signaling adaptor Dab1 to facilitate Reelin signaling. Collectively, these data identify ITSN1 as a component of Reelin signaling that acts predominantly by facilitating the VLDLR-Dab1 axis to direct neuronal migration in the cortex and hippocampus and to augment synaptic plasticity.

scholarly journals Involvement of Receptor-like Protein Tyrosine Phosphatase ζ/RPTPβ and Its Ligand Pleiotrophin/Heparin-binding Growth-associated Molecule (HB-GAM) in Neuronal Migration

1998 ◽  
Vol 142 (1) ◽  
pp. 203-216 ◽  
Author(s):  
Nobuaki Maeda ◽  
Masaharu Noda
Keyword(s):  
Cell Migration ◽  
Chondroitin Sulfate ◽  
Protein Tyrosine Phosphatase ◽  
Neuronal Migration ◽  
Cortical Neurons ◽  
Tyrosine Phosphatase ◽  
Heparin Binding ◽  
Protein Tyrosine ◽  
Radial Glial ◽  
Chondroitin Sulfate A

Pleiotrophin/heparin-binding growth-associated molecule (HB-GAM) is a specific ligand of protein tyrosine phosphatase ζ (PTPζ)/receptor-like protein tyrosine phosphatase β (RPTPβ) expressed in the brain as a chondroitin sulfate proteoglycan. Pleiotrophin and PTPζ isoforms are localized along the radial glial fibers, a scaffold for neuronal migration, suggesting that these molecules are involved in migratory processes of neurons during brain development. In this study, we examined the roles of pleiotrophin-PTPζ interaction in the neuronal migration using cell migration assay systems with glass fibers and Boyden chambers. Pleiotrophin and poly-l-lysine coated on the substratums stimulated cell migration of cortical neurons, while laminin, fibronectin, and tenascin exerted almost no effect. Pleiotrophin-induced and poly-l-lysine–induced neuronal migrations showed significant differences in sensitivity to various molecules and reagents. Polyclonal antibodies against the extracellular domain of PTPζ, PTPζ-S, an extracellular secreted form of PTPζ, and sodium vanadate, a protein tyrosine phosphatase inhibitor, added into the culture medium strongly suppressed specifically the pleiotrophin-induced neuronal migration. Furthermore, chondroitin sulfate C but not chondroitin sulfate A inhibited pleiotrophin-induced neuronal migration, in good accordance with our previous findings that chondroitin sulfate constitutes a part of the pleiotrophin-binding site of PTPζ, and PTPζ-pleiotrophin binding is inhibited by chondroitin sulfate C but not by chondroitin sulfate A. Immunocytochemical analysis indicated that the transmembrane forms of PTPζ are expressed on the migrating neurons especially at the lamellipodia along the leading processes. These results suggest that PTPζ is involved in the neuronal migration as a neuronal receptor of pleiotrophin distributed along radial glial fibers.

Loss of Lgl1 Disrupts the Radial Glial Fiber-guided Cortical Neuronal Migration and Causes Subcortical Band Heterotopia in Mice

Neuroscience ◽  
2019 ◽  
Vol 400 ◽  
pp. 132-145 ◽  
Author(s):  
Tingting Zhang ◽  
Sen Zhang ◽  
Xinli Song ◽  
Xiaohan Zhao ◽  
Congzhe Hou ◽  
...  
Keyword(s):  
Neuronal Migration ◽  
Subcortical Band Heterotopia ◽  
Radial Glial ◽  
Band Heterotopia

Obstructed neuronal migration along radial glial fibers in the neocortex of the reeler mouse: A golgi-EM analysis

1982 ◽  
Vol 4 (4) ◽  
pp. 379-393 ◽  
Author(s):  
M.Cecilia Pinto-Lord ◽  
Philippe Evrard ◽  
Verne S. Caviness
Keyword(s):  
Neuronal Migration ◽  
Radial Glial

scholarly journals Radial Glial Fibers Promote Neuronal Migration and Functional Recovery after Neonatal Brain Injury

2018 ◽  
Vol 22 (1) ◽  
pp. 128-137.e9 ◽  
Author(s):  
Hideo Jinnou ◽  
Masato Sawada ◽  
Koya Kawase ◽  
Naoko Kaneko ◽  
Vicente Herranz-Pérez ◽  
...  
Keyword(s):  
Brain Injury ◽  
Functional Recovery ◽  
Neuronal Migration ◽  
Neonatal Brain ◽  
Neonatal Brain Injury ◽  
Radial Glial

Role of GGF/neuregulin signaling in interactions between migrating neurons and radial glia in the developing cerebral cortex

Development ◽  
1997 ◽  
Vol 124 (18) ◽  
pp. 3501-3510 ◽  
Author(s):  
E.S. Anton ◽  
M.A. Marchionni ◽  
K.F. Lee ◽  
P. Rakic
Keyword(s):  
Cerebral Cortex ◽  
Glial Cells ◽  
Neuronal Migration ◽  
Lipid Binding ◽  
Soluble Form ◽  
Dependent Manner ◽  
Radial Glial Cells ◽  
Glial Development ◽  
Radial Glial

During neuronal migration to the developing cerebral cortex, neurons regulate radial glial cell function and radial glial cells, in turn, support neuronal cell migration and differentiation. To study how migrating neurons and radial glial cells influence each others' function in the developing cerebral cortex, we examined the role of glial growth factor (a soluble form of neuregulin), in neuron-radial glial interactions. Here, we show that GGF is expressed by migrating cortical neurons and promotes their migration along radial glial fibers. Concurrently, GGF also promotes the maintenance and elongation of radial glial cells, which are essential for guiding neuronal migration to the cortex. In the absence of GGF signaling via erbB2 receptors, radial glial development is abnormal. Furthermore, GGF's regulation of radial glial development is mediated in part by brain lipid-binding protein (BLBP), a neuronally induced, radial glial molecule, previously shown to be essential for the establishment and maintenance of radial glial fiber system. The ability of GGF to influence both neuronal migration and radial glial development in a mutually dependent manner suggests that it functions as a mediator of interactions between migrating neurons and radial glial cells in the developing cerebral cortex.

Impairment of radial glial scaffold-dependent neuronal migration and formation of double cortex by genetic ablation of afadin

2015 ◽  
Vol 1620 ◽  
pp. 139-152 ◽  
Author(s):  
Hideaki Yamamoto ◽  
Kenji Mandai ◽  
Daijiro Konno ◽  
Tomohiko Maruo ◽  
Fumio Matsuzaki ◽  
...  
Keyword(s):  
Neuronal Migration ◽  
Genetic Ablation ◽  
Radial Glial ◽  
Double Cortex
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