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  • 1
    Online Resource
    Online Resource
    Expression pattern of the transcription factor Olig2 in response to brain injuries: Implications for neuronal repair
    Proceedings of the National Academy of Sciences ; 2005
    In:  Proceedings of the National Academy of Sciences Vol. 102, No. 50 ( 2005-12-13), p. 18183-18188
    Details
    In: Proceedings of the National Academy of Sciences, Proceedings of the National Academy of Sciences, Vol. 102, No. 50 ( 2005-12-13), p. 18183-18188
    Abstract: Despite the presence of neural stem cells and ongoing neurogenesis in some regions of the adult mammalian brain, neurons are not replaced in most brain regions after injury. With the aim to unravel factors contributing to the failure of neurogenesis in the injured cerebral cortex, we examined the expression of cell fate determinants after acute brain injuries, such as stab wound or focal ischemia, and in a model of chronic amyloid deposition. Although none of the neurogenic factors, such as Pax6, Mash1, Ngn2, was detected in the injured parenchyma, we observed a strong up-regulation of the bHLH transcription factor Olig2, but not Olig1, upon acute and chronic injury. To examine the function of Olig2 in brain lesion, we injected retroviral vectors containing a dominant negative form of Olig2 into the lesioned cortex 2 days after a stab wound. Antagonizing Olig2 function resulted in a significant number of infected cells generating immature neurons that were not observed after injection of the control virus. These data, therefore, imply Olig2 as a repressor of neurogenesis in cells reacting to brain injury and open innovative perspectives toward evoking endogenous neuronal repair.
    Type of Medium: Online Resource
    ISSN: 0027-8424 , 1091-6490
    URL: Article
    DOI: 10.1073/pnas.0506535102
    RVK:
    TA 1000
    RVK:
    WA 15000
    Language: English
    Publisher: Proceedings of the National Academy of Sciences
    Publication Date: 2005
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    detail.hit.zdb_id: 1461794-8
    SSG: 11
    SSG: 12
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  • 2
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    Online Resource
    Origin and progeny of reactive gliosis: A source of multipotent cells in the injured brain
    Proceedings of the National Academy of Sciences ; 2008
    In:  Proceedings of the National Academy of Sciences Vol. 105, No. 9 ( 2008-03-04), p. 3581-3586
    Details
    In: Proceedings of the National Academy of Sciences, Proceedings of the National Academy of Sciences, Vol. 105, No. 9 ( 2008-03-04), p. 3581-3586
    Abstract: Reactive gliosis is the universal reaction to brain injury, but the precise origin and subsequent fate of the glial cells reacting to injury are unknown. Astrocytes react to injury by hypertrophy and up-regulation of the glial-fibrillary acidic protein (GFAP). Whereas mature astrocytes do not normally divide, a subpopulation of the reactive GFAP + cells does so, prompting the question of whether the proliferating GFAP + cells arise from endogenous glial progenitors or from mature astrocytes that start to proliferate in response to brain injury. Here we show by genetic fate mapping and cell type-specific viral targeting that quiescent astrocytes start to proliferate after stab wound injury and contribute to the reactive gliosis and proliferating GFAP + cells. These proliferating astrocytes remain within their lineage in vivo , while a more favorable environment in vitro revealed their multipotency and capacity for self-renewal. Conversely, progenitors present in the adult mouse cerebral cortex labeled by NG2 or the receptor for the platelet-derived growth factor (PDGFRα) did not form neurospheres after (or before) brain injury. Taken together, the first fate-mapping analysis of astrocytes in the adult mouse cerebral cortex shows that some astrocytes acquire stem cell properties after injury and hence may provide a promising cell type to initiate repair after brain injury.
    Type of Medium: Online Resource
    ISSN: 0027-8424 , 1091-6490
    URL: Article
    DOI: 10.1073/pnas.0709002105
    RVK:
    TA 1000
    RVK:
    WA 15000
    Language: English
    Publisher: Proceedings of the National Academy of Sciences
    Publication Date: 2008
    detail.hit.zdb_id: 209104-5
    detail.hit.zdb_id: 1461794-8
    SSG: 11
    SSG: 12
    Location Call Number Limitation Availability
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  • 3
    Online Resource
    Online Resource
    Intensive Remodeling of Purkinje Cell Spines after Climbing Fibers Deafferentation Does Not Involve MAPK and Akt Activation
    Wiley ; 2007
    In:  Annals of the New York Academy of Sciences Vol. 1096, No. 1 ( 2007-01), p. 230-238
    Details
    In: Annals of the New York Academy of Sciences, Wiley, Vol. 1096, No. 1 ( 2007-01), p. 230-238
    Abstract: Abstract :  Subtotal lesion of the inferior olive (IO) achieved by treating experimental animals with 3‐acetylpyridine (3AP) induces partial Purkinje cells (PCs) deafferentation that leads to PC hyperactivity and new spine formation. Coincidentally, the olivary terminals belonging to the few survived olivary neurons undergo an extensive collateral sprouting resulting in reinnervation of the neighboring denervated PCs. We obtained chemical deafferentation of PCs in adult rats (body weight, 120–170 g; age, 35–40 days) by a single intraperitoneal injection of 3AP (65 mg/kg body weight), and as early as 3 days after 3AP treatment, important morphological changes could be observed on PCs. Mitogen‐activated protein kinase (MAPK) cascades and more specifically extracellular signal‐regulated kinases 1/2 (ERK1/2) play a critical role in the signaling events underlying synaptic plasticity. For instance, long‐term depression (LTD) in the adult hippocampus and long‐term potentiation (LTP) in cerebellum both involve ERK activation. Since PCs deprived of their climbing fibers (CFs) afferents initiate an intensive remodeling of the spines and rapid recall of the remaining CFs, it prompted us to see whether the observed phenomena correlated with MAPK and Akt activation . Immunohistochemistry and Western blotting were done at various time points after 3AP application (from 24 h to 6 days), as the exact dynamics of CF loss is not precisely known. As judged by Western blotting, there was no increase of activated ERK in the cerebellum. However, immunohistochemistry revealed increased ERK phosphorylation in the “pinceaux” of basket cells in 3AP animals. Similarly, stress‐activated protein kinase (SAPK)/c‐Jun N‐terminal kinase (JNK), p38 MAPK, and Akt activation were also studied by means of Western blotting and immunohistochemistry. Upon 3AP treatment no changes in phosphorylation status could be seen in the different kinases subjected to analysis. Our results suggest that activation of MAPK and Akt cascades is not essential in this model of neuronal plasticity.
    Type of Medium: Online Resource
    ISSN: 0077-8923 , 1749-6632
    URL: Article
    DOI: 10.1196/annals.1397.089
    RVK:
    TD 7650
    Language: English
    Publisher: Wiley
    Publication Date: 2007
    detail.hit.zdb_id: 2834079-6
    detail.hit.zdb_id: 211003-9
    detail.hit.zdb_id: 2071584-5
    SSG: 11
    Location Call Number Limitation Availability
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  • 4
    Online Resource
    Online Resource
    MAPK Activation in Cerebellar Basket Cell Terminals after Harmaline Treatment
    Wiley ; 2005
    In:  Annals of the New York Academy of Sciences Vol. 1048, No. 1 ( 2005-06), p. 411-417
    Details
    In: Annals of the New York Academy of Sciences, Wiley, Vol. 1048, No. 1 ( 2005-06), p. 411-417
    Abstract: A bstract : The mitogen‐activated protein kinases (MAPKs) are a family of signal transduction mediators that regulate a number of cellular activities, including cell growth and proliferation, differentiation and survival, via phosphorylation (activation) of protein kinases. MAPKs are also recruited during synaptic plasticity and remodeling. In the present study we used Western blotting and immunohistochemistry to examine the effects of harmaline administration on the phosphorylation state of three MAPKs: the extracellular signal‐regulated kinase (ERK1/2), c‐Jun‐N‐terminal kinase/stress‐activated protein kinase (JNK/SAPK), and p38 MAPK. Harmaline is a tremorigenic drug known to induce enhanced and rhythmic firing of the inferior olive. In rats, synchronous activity of the inferior olive cells induced by harmaline administered for four days from postnatal day 9 to 12 resulted in prolonged maintenance of polyinnervation of Purkinje cells by climbing fibers (axons of olivary cells). Immunohistochemistry showed small but sustained cytoplasmic positivity to phospho‐ERK in Purkinje cells and a strong signal for phospho‐ERK in the “pinceaux,” terminals of the interneuronal basket cells onto Purkinje cells. A similar pattern was observed for/JNK/SAPK, while no changes in p38 were noticed. Thus, it was revealed that the activation of two members of the MAPK family in these inhibitory presynaptic terminals is also one consequence of synchronous olivary input to Purkinje cells known to affect developmental plasticity.
    Type of Medium: Online Resource
    ISSN: 0077-8923 , 1749-6632
    URL: Article
    DOI: 10.1196/annals.1342.051
    RVK:
    TD 7650
    Language: English
    Publisher: Wiley
    Publication Date: 2005
    detail.hit.zdb_id: 2834079-6
    detail.hit.zdb_id: 211003-9
    detail.hit.zdb_id: 2071584-5
    SSG: 11
    Location Call Number Limitation Availability
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