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Neurogenic Regions (neurogenic + regions)

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Life Sciences	100%

Selected Abstracts

Extracerebellar progenitors grafted to the neurogenic milieu of the postnatal rat cerebellum adapt to the host environment but fail to acquire cerebellar identities

EUROPEAN JOURNAL OF NEUROSCIENCE, Issue 8 2010
Chiara Rolando
Abstract Stem or progenitor cells acquire specific regional identities during early ontogenesis. Nonetheless, there is evidence that cells heterotopically transplanted to neurogenic regions of the developing or mature central nervous system may switch their fate to adopt host-specific phenotypes. Here, we isolated progenitor cells from different germinative sites along the neuraxis where GABAergic interneurons are produced (telencephalic subventricular zone, medial ganglionic eminence, ventral mesencephalon and dorsal spinal cord), and grafted them to the prospective white matter of the postnatal rat cerebellum, at the time when local interneurons are generated. The phenotype acquired by transplanted cells was assessed by different criteria, including expression of region-specific transcription factors, acquisition of morphological and neurochemical traits, and integration in the cerebellar cytoarchitecture. Regardless of their origin, all the different types of donor cells engrafted in the cerebellar parenchyma and developed mature neurons that shared some morphological and neurochemical features with local inhibitory interneurons, particularly in the deep nuclei. Nevertheless, transplanted cells failed to activate cerebellar-specific regulatory genes. In addition, their major structural features, the expression profiles of type-specific markers and the laminar placement in the recipient cortex did not match those of endogenous interneurons generated during the same developmental period. Therefore, although exogenous cells are influenced by the cerebellar milieu and show remarkable capabilities for adapting to the foreign environment, they essentially fail to switch their fate, integrate in the host neurogenic mechanisms and adopt clear-cut cerebellar identities. [source]

Glycine cleavage system in neurogenic regions

EUROPEAN JOURNAL OF NEUROSCIENCE, Issue 9 2004
Akiko Ichinohe
Abstract The glycine cleavage system (GCS) is the essential enzyme complex for degrading glycine and supplying 5,10-methylenetetrahydrofolate for DNA synthesis. Inherited deficiency of this system causes nonketotic hyperglycinemia, characterized by severe neurological symptoms and frequent association of brain malformations. Although high levels of glycine have been considered to cause the above-mentioned problems, the detailed pathogenesis of this disease is still unknown. Here we show that GCS is abundantly expressed in rat embryonic neural stem/progenitor cells in the neuroepithelium, and this expression is transmitted to the radial glia,astrocyte lineage, with prominence in postnatal neurogenic regions. These data indicate that GCS plays important roles in neurogenesis, and suggest that disturbance of neurogenesis induced by deficiency of GCS may be the main pathogenesis of nonketotic hyperglycinemia. [source]

Chemokine receptor expression by neural progenitor cells in neurogenic regions of mouse brain

THE JOURNAL OF COMPARATIVE NEUROLOGY, Issue 6 2007
Phuong B. Tran
Abstract We previously demonstrated that chemokine receptors are expressed by neural progenitors grown as cultured neurospheres. To examine the significance of these findings for neural progenitor function in vivo, we investigated whether chemokine receptors were expressed by cells having the characteristics of neural progenitors in neurogenic regions of the postnatal brain. Using in situ hybridization we demonstrated the expression of CCR1, CCR2, CCR5, CXCR3, and CXCR4 chemokine receptors by cells in the dentate gyrus (DG), subventricular zone of the lateral ventricle, and olfactory bulb. The pattern of expression for all of these receptors was similar, including regions where neural progenitors normally reside. In addition, we attempted to colocalize chemokine receptors with markers for neural progenitors. In order to do this we used nestin-EGFP and TLX-LacZ transgenic mice, as well as labeling for Ki67, a marker for dividing cells. In all three areas of the brain we demonstrated colocalization of chemokine receptors with these three markers in populations of cells. Expression of chemokine receptors by neural progenitors was further confirmed using CXCR4-EGFP BAC transgenic mice. Expression of CXCR4 in the DG included cells that expressed nestin and GFAP as well as cells that appeared to be immature granule neurons expressing PSA-NCAM, calretinin, and Prox-1. CXCR4-expressing cells in the DG were found in close proximity to immature granule neurons that expressed the chemokine SDF-1/CXCL12. Cells expressing CXCR4 frequently coexpressed CCR2 receptors. These data support the hypothesis that chemokine receptors are important in regulating the migration of progenitor cells in postnatal brain. J. Comp. Neurol. 500:1007,1033, 2007. © 2006 Wiley-Liss, Inc. [source]

Expression of synapsin III in nerve terminals and neurogenic regions of the adult brain

THE JOURNAL OF COMPARATIVE NEUROLOGY, Issue 2 2002
Vincent A. Pieribone
Abstract We have examined the distribution of synapsin III in the adult mouse brain. Expression of synapsin III was observed in puncta throughout the brain, but demonstrated greater regional variation than that of synapsins I or II. This punctate staining is typical for synaptic vesicle proteins located at nerve terminals. These findings are also consistent with the well-established role for synapsins in regulating neurotransmitter release. However, unexpectedly, synapsin III was also highly expressed in the cell body and processes of immature neurons in neurogenic regions of the adult brain, such as the hippocampal dentate gyrus, rostral migratory stream, and olfactory bulb. Many synapsin III-positive neurons also reacted with an antibody directed toward polysialylated-neuronal cell adhesion molecule, a marker of immature, migrating neurons. These results suggest that synapsin III may also play a role in adult neurogenesis. J. Comp. Neurol. 454:105,114, 2002. © 2002 Wiley-Liss, Inc. [source]