**Author details**

Jenny Wong1,2

Address all correspondence to: jwong@uow.edu.au

1 Illawarra Health and Medical Research Institute, University of Wollongong, Wollongong, NSW, 2522, Australia

2 School of Biological Sciences, University of Wollongong, Wollongong, NSW, 2522, Austral‐ ia

#### **References**

[1] Schindowski K, Belarbi K, and Buee L. Neurotrophic factors in Alzheimer's disease: role of axonal transport. Genes, Brain, and Behavior 2008;7 Suppl 143-56.

[2] Patapoutian A and Reichardt LF. Trk receptors: mediators of neurotrophin action. Current Opinion in Neurobiology 2001;11(3) 272-280.

**5. Conclusion**

190 Trends in Cell Signaling Pathways in Neuronal Fate Decision

**Nomenclature**

tor kinase).

**Acknowledgements**

back on the chapter drafts.

Address all correspondence to: jwong@uow.edu.au

**Author details**

NSW, 2522, Australia

Jenny Wong1,2

**References**

ia

Neurotrophin signaling via BDNF/TrkB-TK+ is critical for neuronal viability and function. Further research into this topic area is required to determine when changes in BDNF/TrkB-TK+ signaling begin to occur and whether changes in TrkB-Shc expression, function, and in‐ teraction with TrkB-TK+ at different stages of the disease process, in response to Aβ, or in

Aβ (amyloid beta), AD (Alzheimer's disease), Akt (protein kinase B), BDNF (brain-de‐ rived neurotrophic factor), CA1 (Cornu Ammonis area 1), CHO (Chinese hamster ovary), ERK (extracellular signal-regulated kinase), MEK (mitogen-activated protein kinase kin‐ ase), NGF (nerve growth factor), NT (neurotrophin), PI3K (phosphatidyl inositol 3 kinase), PLCγ (phospholipase C-gamma), Shc (sarc homology containing), Trk (tropomyosin recep‐

Many thanks to Dr John BJ Kwok from Neuroscience Research Australia for providing feed‐

1 Illawarra Health and Medical Research Institute, University of Wollongong, Wollongong,

2 School of Biological Sciences, University of Wollongong, Wollongong, NSW, 2522, Austral‐

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**Section 4**

**NF-K-b and Neuronal Fate Decision**

**NF-K-b and Neuronal Fate Decision**

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194 Trends in Cell Signaling Pathways in Neuronal Fate Decision

**Chapter 8**

**NFκB Signaling Directs Neuronal Fate Decision**

During neural induction, the ectoderm stem cells overlying the notochord of the mesoderm convert into neuroepithelial cells (NECs) that proliferate/differentiate rapidly to form neural plate in response to diffusible inhibitory signals (neural inducer) produced from the noto‐ chord. Neural plate folds to form neural groove, which fuses to form neural tube. Within the neural tube, NECs undergo asymmetric dividing to generate neural stem cells (NSCs, or called radial glia cells) due to the expression of B-cell translocation gene 2 (BTG2) [1, 2, 3, 4]. NSCs differentiate sequentially into neural progenitor cells (NPCs) and various lineage-re‐ stricted neural blast cells, which include neuroblast and glioblast. These neural blast cells migrate to the target region where they mature and integrate into the existing neural net‐ work [5]. The generation of different lineage occurs in a temporally distinct yet overlapping pattern. In rodents, neuronogenesis peaks at embryonic day (E) 14, astrocytogenesis at post‐ natal day (P) 2, and oligodendrocytogenesis at P14 [6, 7]. It remains largely unclear at which step the fate of neuronal lineage has been decided, from embryonic stem (ES) cells to NECs, to NSCs and to terminally-differentiated neurons. The transcriptional factor NFκB plays a pivotal role in inflammation, immunity, cancer and neural plasticity [8, 9]. Constitutive and inducible activation of NFκB has been reported in many types of human tumors and chronic diseases including neurodegenerative diseases [10, 11, 12, 13, 14]. However, moderate acti‐ vation of NFκB signaling on many physiological conditions may benefit the whole process

of neuronal fate decision, including neurodevelopment and adult neurogenesis [15].

**2. NFκB initiates and maintains neuronal fate decision from neural stem**

NFκB is activated through a series of signaling cascades (Figure 1). The NFκB family con‐ tains 5 members including RelA(p65), RelB, c-Rel, p50/p105 (NFκB1) and p52/p100 (NFκB2),

> © 2013 Zhang and Hu; licensee InTech. This is an open access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

© 2013 Zhang and Hu; licensee InTech. This is a paper distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Yonggang Zhang and Wenhui Hu

http://dx.doi.org/10.5772/53503

**1. Introduction**

**cells**

Additional information is available at the end of the chapter
