Neural Cell Proliferation (neural + cell_proliferation)

Distribution by Scientific Domains


Selected Abstracts


An olig2 reporter gene marks oligodendrocyte precursors in the postembryonic spinal cord of zebrafish

DEVELOPMENTAL DYNAMICS, Issue 12 2007
Hae-Chul Park
Abstract Continuous production of new neurons and glia in adult mammals occurs within specialized proliferation zones of the forebrain. Neural cell proliferation and neurogenesis is more widespread in adult amphibians, reptiles, and fish but the identity of neural stem cell populations in these organisms has not been fully described. We investigated expression of a reporter gene driven by olig2 regulatory DNA at postembryonic stages in zebrafish. We show that olig2 expression marks a discrete population of spinal cord radial glia in larvae and adults that divide continuously. olig2+ radial glia have hallmarks of stem cells and their divisions appear to be asymmetric, producing new oligodendrocytes but not neurons or astrocytes. Developmental Dynamics 236:3402,3407, 2007. © 2007 Wiley-Liss, Inc. [source]


The importance of cerebrospinal fluid on neural cell proliferation in developing chick cerebral cortex

EUROPEAN JOURNAL OF NEUROLOGY, Issue 3 2006
F. Mashayekhi
Cerebrospinal fluid (CSF) is mainly produced by the choroid plexuses within the ventricles of the brain. The CSF circulates in a regular manner after the ventricular system and the choroids plexuses have developed, and the foramina in the fourth ventricle have opened to enable it to carry chemical information. CSF flows through the ventricular system passing over all regions of germinal activity. In this study, chick embryos were used to show the importance of CSF on neural cell proliferation in the developing cerebral cortex. The chick embryos were cannulated in situ with a fine capillary tube to drain CSF out of the ventricular system. At the same time, BrdU was administered to the embryos. After surgery the embryos were incubated for another 3 days. Quantitative measurements showed that the thicknesses of the germinal epithelium and cerebral cortex in CSF-drained embryos were less than those in the control group at the same age. The number of cells produced in the germinal epithelium of CSF-drained embryos was decreased when compared with the normal group. This study provides confirmatory evidence that CSF is important for neural cell proliferation and therefore normal development of the cerebral cortex. It is proposed that CSF is vital in controlling development of the cerebral cortex. [source]


Neuropeptide Y stimulates retinal neural cell proliferation , involvement of nitric oxide

JOURNAL OF NEUROCHEMISTRY, Issue 6 2008
Ana Rita Álvaro
Abstract Neuropeptide Y (NPY) is a 36 amino acid peptide widely present in the CNS, including the retina. Previous studies have demonstrated that NPY promotes cell proliferation of rat post-natal hippocampal and olfactory epithelium precursor cells. The aim of this work was to investigate the role of NPY on cell proliferation of rat retinal neural cells. For this purpose, primary retinal cell cultures expressing NPY, and NPY Y1, Y2, Y4 and Y5 receptors [Álvaro et al., (2007) Neurochem. Int., 50, 757] were used. NPY (10,1000 nM) stimulated cell proliferation through the activation of NPY Y1, Y2 and Y5 receptors. NPY also increased the number of proliferating neuronal progenitor cells (BrdU+/nestin+ cells). The intracellular mechanisms coupled to NPY receptors activation that mediate the increase in cell proliferation were also investigated. The stimulatory effect of NPY on cell proliferation was reduced by l -nitroarginine-methyl-esther (l -NAME; 500 ,M), a nitric oxide synthase inhibitor, 1H-[1,2,4]oxadiazolo-[4, 3-a]quinoxalin-1-one (ODQ; 20 ,M), a soluble guanylyl cyclase inhibitor or U0126 (1 ,M), an inhibitor of the extracellular signal-regulated kinase 1/2 (ERK 1/2). In conclusion, NPY stimulates retinal neural cell proliferation, and this effect is mediated through nitric oxide,cyclic GMP and ERK 1/2 pathways. [source]


Interactions between neural membrane glycerophospholipid and sphingolipid mediators: A recipe for neural cell survival or suicide

JOURNAL OF NEUROSCIENCE RESEARCH, Issue 9 2007
Akhlaq A. Farooqui
Abstract The neural membranes contain phospholipids, sphingolipids, cholesterol, and proteins. Glycerophospholipids and sphingolipids are precursors for lipid mediators involved in signal transduction processes. Degradation of glycerophospholipids by phospholipase A2 (PLA2) generates arachidonic acid (AA) and docosahexaenoic acids (DHA). Arachidonic acid is metabolized to eicosanoids and DHA is metabolized to docosanoids. The catabolism of glycosphingolipids generates ceramide, ceramide 1-phosphate, sphingosine, and sphingosine 1-phosphate. These metabolites modulate PLA2 activity. Arachidonic acid, a product derived from glycerophospholipid catabolism by PLA2, modulates sphingomyelinase (SMase), the enzyme that generates ceramide and phosphocholine. Furthermore, sphingosine 1-phosphate modulates cyclooxygenase, an enzyme responsible for eicosanoid production in brain. This suggests that an interplay and cross talk occurs between lipid mediators of glycerophospholipid and glycosphingolipid metabolism in brain tissue. This interplay between metabolites of glycerophospholipid and sphingolipid metabolism may play an important role in initiation and maintenance of oxidative stress associated with neurologic disorders as well as in neural cell proliferation, differentiation, and apoptosis. Recent studies indicate that PLA2 and SMase inhibitors can be used as neuroprotective and anti-apoptotic agents. Development of novel inhibitors of PLA2 and SMase may be useful for the treatment of oxidative stress, and apoptosis associated with neurologic disorders such as stroke, Alzheimer disease, Parkinson disease, and head and spinal cord injuries. © 2007 Wiley-Liss, Inc. [source]