Scientific Institute of the Cavalieri Ottolenghi Foundation

Sant'Ambrogio di Torino, Italy

Scientific Institute of the Cavalieri Ottolenghi Foundation

Sant'Ambrogio di Torino, Italy
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Buffo A.,University of Turin | Buffo A.,Scientific Institute of the Cavalieri Ottolenghi Foundation
Archives Italiennes de Biologie | Year: 2010

In the adult murine central nervous system (CNS), the germinal astroglia residing in the subependymal zone of the lateral ventricles and in the subgranular layer of the hippocampal dentate gyrus behaves as neural stem cells actively undergoing neurogenesis and gliogenesis. Although neurogenesis does not normally occur outside the germinal niches, two types of parenchymal glial cells, namely astrocytes and NG2-expressing cells, display distinct progenitor activities in the intact brain or upon injury. Importantly, in defined experimental conditions both cell types reveal the potential to behave as multipotent stem cells suggesting that the mature CNS parenchyma may retain a latent stem cell potential, normally inhibited in vivo that, if properly evoked, might be exploited in situ for endogenous cell replacement following injury. In this review we scrutinise recent studies focussing on (i) the molecular and functional relationships between precursors in germinal niches and non-germinal areas; (ii) the ability of adult parenchymal glia to undergo lineage transgressions and neurogenesis in the intact brain and upon CNS injury. We also compare evidence for lineage plasticity in astrocytes or NG2+ cells, and discuss possible approaches for the implementation of stem/progenitor cell capabilities in non-germinal glial cells.

Martini M.,University of Turin | Miceli D.,University of Turin | Gotti S.,University of Turin | Viglietti-Panzica C.,University of Turin | And 6 more authors.
Journal of Neuroendocrinology | Year: 2010

Bisphenol A (BPA) is a well-known plastic-derived pollutant that can bind to oestrogen receptors and is considered an endocrine-disrupting chemical. Its impact on different behaviours in rodents has been largely investigated, however, only a few data are available on its effects upon neural circuits. In the present study, we investigated the long-term effects of early exposure of mice of both sexes to BPA on the nitrinergic system, one of the neural systems involved in the control of sexual behaviour and under the control of gonadal hormones. Mice of both sexes were exposed for eight prenatal and eight postnatal days to BPA that was administered to the mothers. The maternally-exposed mice were sacrificed at the age of 2 months and their brains were sectioned and immunohistochemically treated for the detection of neuronal nitric oxide synthase (nNOS). Significant effects of BPA exposure were detected for the number of immunoreactive cells in the medial preoptic nucleus and in the ventromedial subdivision of the bed nucleus of the stria terminalis, in a sex-oriented and dose-dependent way. These results indicate that BPA has a powerful effect on specific portions of the nNOS-immunoreactive system belonging to the accessory olfactory system that are particularly important for the control of sexual behaviour. In addition, they confirm that perinatal exposure to endocrine-disrupting chemicals, in particular to BPA, may have a high impact on the organisation of specific neural pathways that can later affect complex behaviours and functions. © 2010 The Authors. Journal of Neuroendocrinology © 2010 Blackwell Publishing Ltd.

Luzzati F.,University of Turin | Luzzati F.,Scientific Institute of the Cavalieri Ottolenghi Foundation | de Marchis S.,University of Turin | Parlato R.,German Cancer Research Center | And 5 more authors.
PLoS ONE | Year: 2011

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 Camkcre4Crem -/- 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. © 2011 Luzzati et al.

Guglielmotto M.,University of Turin | Aragno M.,University of Turin | Tamagno E.,University of Turin | Tamagno E.,Scientific Institute of the Cavalieri Ottolenghi Foundation | And 9 more authors.
Neurobiology of Aging | Year: 2012

Although the pathogenesis of sporadic Alzheimer disease (AD) is not clearly understood, it is likely dependent on several age-related factors. Diabetes is a risk factor for AD, and multiple mechanisms connecting the 2 diseases have been proposed. Hyperglycemia enhances the formation of advanced glycation end products (AGEs) that result from the auto-oxidation of glucose and fructose. The interaction of AGEs with their receptor, named RAGE, elicits the formation of reactive oxygen species that are also believed to be an early event in AD pathology. To investigate a functional link between the disorders diabetes and AD, the effect of 2 AGEs, pentosidine and glyceraldehydes-derived pyridinium (GLAP), was studied on BACE1 expression both in vivo, in streptozotocin treated rats, and in vitro in differentiated neuroblastoma cells. We showed that pentosidine and GLAP were able to upregulate BACE1 expression through their binding with RAGE and the consequent activation of NF-κB. In addition, both pentosidine and GLAP were found to be increased in the brain in sporadic AD patients. Our findings demonstrate that activation of the AGEs/RAGE axis, by upregulating the key enzyme for amyloid-β production, provides a pathologic link between diabetes mellitus and AD. © 2012 Elsevier Inc.

Carulli D.,University of Cambridge | Carulli D.,Scientific Institute of the Cavalieri Ottolenghi Foundation | Pizzorusso T.,CNR Institute of Neuroscience | Pizzorusso T.,University of Florence | And 8 more authors.
Brain | Year: 2010

Chondroitin sulphate proteoglycans in the extracellular matrix restrict plasticity in the adult central nervous system and their digestion with chondroitinase reactivates plasticity. However the structures in the extracellular matrix that restrict plasticity are unknown. There are many changes in the extracellular matrix as critical periods for plasticity close, including changes in chondroitin sulphate proteoglycan core protein levels, changes in glycosaminoglycan sulphation and the appearance of dense chondroitin sulphate proteoglycan-containing perineuronal nets around many neurons. We show that formation of perineuronal nets is triggered by neuronal production of cartilage link protein Crtl1 (Hapln1), which is up-regulated in the visual cortex as perineuronal nets form during development and after dark rearing. Mice lacking Crtl1 have attenuated perineuronal nets, but the overall levels of chondroitin sulphate proteoglycans and their pattern of glycan sulphation are unchanged. Crtl1 knockout animals retain juvenile levels of ocular dominance plasticity and their visual acuity remains sensitive to visual deprivation. In the sensory pathway, axons in knockout animals but not controls sprout into the party denervated cuneate nucleus. The organization of chondroitin sulphate proteoglycan into perineuronal nets is therefore the key event in the control of central nervous system plasticity by the extracellular matrix. © 2010 The Author.

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