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TrkB regulates neocortex formation through the Shc/PLCγ‐mediated control of neuronal migration
Author(s) -
Medina Diego L,
Sciarretta Carla,
Calella Anna Maria,
von Bohlen und Halbach Oliver,
Unsicker Klaus,
Minichiello Liliana
Publication year - 2004
Publication title -
the embo journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 7.484
H-Index - 392
eISSN - 1460-2075
pISSN - 0261-4189
DOI - 10.1038/sj.emboj.7600399
Subject(s) - tropomyosin receptor kinase b , neocortex , biology , neuroscience , receptor tyrosine kinase , low affinity nerve growth factor receptor , tropomyosin receptor kinase c , cerebral cortex , microbiology and biotechnology , tropomyosin receptor kinase a , neurotrophin , signal transduction , receptor , neurotrophic factors , genetics , platelet derived growth factor receptor , growth factor
The generation of complex neuronal structures, such as the neocortex, requires accurate positioning of neurons and glia within the structure, followed by differentiation, formation of neuronal connections, and myelination. To understand the importance of TrkB signaling during these events, we have used conditional and knockin mutagenesis of the TrkB neurotrophin receptor, and we now show that this tyrosine kinase receptor, through docking sites for the Shc/FRS2 adaptors and phospholipase Cγ (PLCγ), coordinates these events in the cerebral cortex by (1) controlling cortical stratification through the timing of neuronal migration during cortex formation, and (2) regulating both neuronal and oligodendrocyte differentiation. These results provide genetic evidence that TrkB regulates important functions throughout the formation of the cerebral cortex via recruitment of the Shc/FRS2 adaptors and PLCγ.