Cortical Development: From Specification to Differentiation by Richard S. Nowakowski, Verne S. Caviness Jr, Takao Takahashi

By Richard S. Nowakowski, Verne S. Caviness Jr, Takao Takahashi (auth.), Dr. Christine Hohmann (eds.)

The cerebral neocortex, a constitution exact to the mammalian mind and prerequisite for better cognitive capabilities, has considering that many years attracted the interest of neurobiologists and developmental biologists alike. This quantity supplies a accomplished and updated evaluation of early cortical improvement. It presents concise info at the delivery, specification, migration and terminal differentiation of neocortical cells. either the mobile and molecular occasions resulting in the institution of a useful neocortex are provided in enormous aspect, and attainable implications for neurodegenerative illnesses are discussed.

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1997; Murtagh et al. 1999; Zhu et al. 1999b). Shh also interacts with FGF and Wnt developmental signaling pathways (Hirsinger et al. 1997; Marcelle et al. 1997; Zuniga et al. 1999). FGF and Shh exhibit co operative effects to promote the elaboration of specific regional neuronal subtypes (Ye et al. 1998). Further, BMPs can potentiate and Shh can inhibit the activities of the Wnt signaling pathway (Marcelle et al. 1997). In addition to Shh, Wnt signaling can also potentiate the expression of the BMP antagonist, noggin (Hirsinger et al.

2001). The continued rise in GI and Q despite the fall in p27 Kip1 indicates that other molecules must come into play during the third phase. This means that other cell cyde regulators are probably involved (Zindy et al. 1999; Cunningham and RousseI2001). In addition, it has been shown that growth factors and other small molecules, induding FGF2 (Ghosh and Greenberg 1995; Vaccarino et al. 1999a,b; Raballo et al. 2000), PACAP (Nicot and DiCicco-Bloom 2001; Suh et al. 2001), IGF-l (Drago et al. 1991), and NT3 (Ghosh and Greenberg 1995), may all playa role either as amitogen or an anti-mitogen.

1999). These factors can differentially regulate the stoichiometry of neurogenic bHLH factors by preferentially binding to and sequestering a subset of ubiquitous bHLH proteins, thereby preventing these molecules from forming appropriate heterodimers with cell-type-specific neurogenic bHLH factors that normally promote early neurogenesis (Norton et al. 1998; Sasai 1998; Bounpheng et al. 1999; Lyden et al. 1999). The proliferation, survival and differentiation of NSCs and nascent progenitor species are regulated by specific cytokines, induding epidermal growth factor (EGF) and bFGF (Kilpatrick and Bartlett 1995; Kilpatrick et al.

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