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  • 1
    Keywords: IN-VITRO ; SURVIVAL ; human ; INHIBITION ; VITRO ; SYSTEM ; PROTEIN ; transcription ; DIFFERENTIATION ; MICE ; TRANSCRIPTION FACTOR ; PHOSPHORYLATION ; ELEMENT-BINDING PROTEIN ; NERVOUS-SYSTEM ; TRANSCRIPTION FACTORS ; TRANSGENIC MICE ; immunohistochemistry ; MIGRATION ; PROGENITOR CELLS ; TRACER ; ADULT ; MICE LACKING ; NEURONS ; cell survival ; SPINE ; development ; PHASE ; ADULT MAMMALIAN BRAIN ; adult neurogenesis ; cell differentiation ; CREB PHOSPHORYLATION ; downregulation ; GENERATED NEURONS ; NEURONAL DIFFERENTIATION ; olfactory deafferentation ; PHENOTYPIC DIFFERENTIATION ; radial migration ; SUBEPENDYMAL ZONE ; SUBVENTRICULAR ZONE
    Abstract: The transcription factor cAMP response element-binding protein ( CREB) is involved in multiple aspects of neuronal development and plasticity. Here, we demonstrate that CREB regulates specific phases of adult neurogenesis in the subventricular zone/olfactory bulb (SVZ/OB) system. Combining immunohistochemistry with bromodeoxyuridine treatments, cell tracer injections, cell transplants, and quantitative analyses, we show that although CREB is expressed by the SVZ neuroblasts throughout the neurogenic process, its phosphorylation is transient and parallels neuronal differentiation, increasing during the late phase of tangential migration and decreasing after dendrite elongation and spine formation. In vitro, inhibition of CREB function impairs morphological differentiation of SVZ-derived neuroblasts. Transgenic mice lacking CREB, in a null CREM genetic background, show reduced survival of newborn neurons in the OB. This finding is further supported by peripheral afferent denervation experiments resulting in downregulation of CREB phosphorylation in neuroblasts, the survival of which appears heavily impaired. Together, these findings provide evidence that CREB regulates differentiation and survival of newborn neurons in the OB
    Type of Publication: Journal article published
    PubMed ID: 16267218
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  • 2
    Keywords: EXPRESSION ; POPULATION ; DIFFERENTIATION ; MICE ; MIGRATION ; PROGENITOR CELLS ; QUANTITATIVE-ANALYSIS ; NEURAL STEM-CELLS ; ADULT BRAIN ; FOREBRAIN NEUROGENESIS ; ISCHEMIC BRAIN-INJURY ; MUTANT HUNTINGTIN ; OLFACTORY-BULB INTERNEURONS
    Abstract: Acute striatal lesions increase proliferation in the subventricular zone (SVZ) and induce migration of SVZ neuroblasts to the striatum. However, the potential of these cells to replace acutely degenerated neurons is controversial. The possible contribution of parenchymal progenitors to striatal lesion-induced neurogenesis has been poorly explored. Here, we present a detailed investigation of neurogenesis in the striatum of a mouse model showing slow progressive neurodegeneration of striatal neurons, the Creb1(Camkcre4) Crem(-/-) mutant mice (CBCM). By using BrdU time course analyses, intraventricular injections of a cell tracker and 3D reconstructions we showed that neurodegeneration in CBCM mice stimulates the migration of SVZ neuroblasts to the striatum without altering SVZ proliferation. SVZ-neuroblasts migrate as chains through the callosal striatal border and then enter within the striatal parenchyma as individual cells. In addition, a population of clustered neuroblasts showing high turnover rates were observed in the mutant striatum that had not migrated from the SVZ. Clustered neuroblasts might originate within the striatum itself because they are specifically associated with parenchymal proliferating cells showing features of intermediate neuronal progenitors such as clustering, expression of EGF receptor and multiple glial (SOX2, SOX9, BLBP) and neuronal (Dlx, Sp8, and to some extent DCX) markers. Newborn striatal neurons had a short lifespan and did not replace projection neurons nor expressed sets of transcription factors involved in their specification. The differentiation failure of endogenous neuroblasts likely occurred cell autonomously because transplanted wild type embryonic precursors correctly differentiated into striatal projection neurons. Thus, we propose that under progressive degeneration, neither SVZ derived nor intra-striatal generated neurons have the potential to differentiate into striatal projection neurons
    Type of Publication: Journal article published
    PubMed ID: 21980380
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  • 3
    ISSN: 1460-9568
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Olfactory bulb interneurons are continuously generated throughout development and in adulthood. These neurons are born in the subventricular zone (SVZ) and migrate along the rostral migratory stream into the olfactory bulb where they differentiate into local interneurons. To investigate the differentiation of GABAergic interneurons of the olfactory bulb we used a transgenic mouse which expresses green fluorescent protein (GFP) under the control of the glutamic acid decarboxylase 65 kDa (GAD65) promoter. During development and in adulthood GFP was expressed by cells in the SVZ and along the entire length of its rostral extension including the distal portion within the olfactory bulb. The occurrence of GAD65 mRNA in these zones was confirmed by PCR analysis on microdissected regions along the pathway. Polysialic acid neural cell adhesion molecule, a marker of migrating neuroblasts in adults, was coexpressed by the majority of the GFP-positive SVZ-derived progenitor cells. Cell tracer injections into the SVZ indicated that ≈ 26% of migrating progenitor cells expressed GFP. These data show the early differentiation of migrating SVZ-derived progenitors into a GAD65–GFP-positive phenotype. These cells could represent a restricted lineage giving rise to GAD65-positive GABAergic olfactory bulb interneurons.
    Type of Medium: Electronic Resource
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  • 4
    ISSN: 0960-0760
    Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics: Biology , Chemistry and Pharmacology
    Type of Medium: Electronic Resource
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