Neural development

Semaphorins are secreted, membrane-associated or transmembrane proteins defined by the presence of a sema-phorin protein domain (Serna domain). In the mammalian system, more than 20 semaphorins have been identified which play important roles in a variety of tissues. The best characterized receptors for mediating semaphoiin effects are members of the neuropilin and plexin families of transmembrane proteins. Semaphoiin functions are best described in the regulation of neural development, angiogenesis, immunoregulation and cancer. 

Brimijoin S, Koenigsberger C. 1999. Cholinesterases in neural development New findings and toxicologic implications. Environ Health Perspect 107 (Supp. l) 59-64. 

Finally, entry of Ca + through somatic and dendritic Ca + channels activates calmodulin-dependent protein kinases to modulate transcription, and thereby plays a crucial role in certain components of neural development and plasticity. 

A variety of substrate- and cell-attached factors influence neural development by regulating adhesion properties of cells (see Ch. 7). Interactions occur directly between cells or between a cell and the extracellular matrix (see Ch. 2). The molecules mediating these interactions have been implicated in regulating the specificity and timing of cell-cell adhesion and the consequences on cell morphology and physiology. Hence, they influence the ability of cells not only to migrate but to sort themselves out and to stabilize spatial relationships considered important for the process of differentiation. 

The FGFs stimulate the proliferation of mesodermally and ectodermally-derived cells and play central roles in mammalian development. Members of the FGF family are expressed in the embryonic period and are required for several critical events in neural development and specifically for neural induction. FGF-8 is necessary for positional identity required for axial specification and patterning of limb development. FGF-2 stimulates the proliferation of multipotential stem cells that subsequently give rise to neurons of the cortex and other brain regions. 

Baloh, R. H., Enomoto, H., Johnson, E. M. Jr and Milbrandt, J. The GDNF family ligands and receptors - implications for neural development. Curr. Opin. Neurobiol. 10 103-110, 2000. 

De la Rosa, E. J. and de Pablo, F. Cell death in early neural development beyond the neurotrophic theory. Trends Neurosci. 23 454-458, 2000. 

Cameron, H. A. and Gould, E. The control of neuronal birth and survival. In Receptor Dynamics in Neural Development (1st edn). Ed. Shaw, C. A. New York CRC Press, 1996, ppl41-157. 

Suzuki, M., et al., Xenopus laevis macrophage migration inhibitory factor is essential for axis formation and neural development, J. Biol. Chem., 279, 21406, 2004. 

The effect of elevated extracellular 5-HT concentration on the modulation of programmed cell death during neural development was also investigated in early postnatal brains of 5-HTT KO mice. 5-HTT gene inactivations leads to a reduced number of apoptotic cells in striatum, thalamus, hypothalamus. 

Goodman, C.S., and Tessier-Lavigne, M. (1997) Molecular mechanisms to axin guidance and target recognition. In (Cowan, W.M., Jessel, T.M., and Zipursky, S.L., eds). Molecular and Cellular Approaches to Neural Development, 1st ed. New York Oxford University Press, pp. 108-178. 

Reichardt, L.F., and Tomaselli, K.J. (1991) Extracellular matrix molecules and their receptors functions in neural development. Ann Rev Neurosci 14 531-570. 

The psychiatric community, the lay press, and ads on the Internet have drawn attention to the role of essential fatty acids (EFAs) on neural development and on the treatment of mental illness. The EFAs are often referred to as omega-3 and omega-6 fatty acids, and include fish oil, flax seed oil, and evening primrose oil supplements. 

Berenbaum, S. (1998) How hormones affect behavioral and neural development gonadal hotmones and sex differences. Dev Neu-ropsychol 14 175—196. 

Laabs, T., Carulli, D., Geller, H. M., and Fawcett, J. W. (2005). Chondroitin sulfate proteoglycans in neural development and regeneration. Curr. Opin. Neurobiol. 15,116-120. 

T Given that many amino acids are either neurotransmitters or precursors or antagonists of neutrotransmitters, genetic defects of amino acid metabolism can cause defective neural development and mental retardation. In most such diseases specific intermediates accumulate. For example, a genetic defect in phenylalanine hydroxylase, the first enzyme in the catabolic pathway for phenylalanine (Fig. 18-23), is responsible for the disease phenylketonuria (PKU), the most common cause of elevated levels of phenylalanine (hyperphenylalaninemia). 

Chen C. and Tonegawa S. (1997). Molecular genetic analysis of synaptic plasticity, activity-dependent neural development, learning, and memory in the mammalian brain. Annu. Rev. Neurosci. 20 157-184. 

Only RSD has been studied in neonates. Three reasons may apply (a) REM sleep may have more attraction for its special feature as a driving force for neural development. (b) REM sleep occupies about 70% of time followed by wakefulness, and NREM sleep occupies only a very small proportion of daily behavior, (c)... 

---