Inactivation of bcl-2 results in progressive degeneration of motoneurons, sympathetic and sensory neurons during early postnatal development

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dc.contributor.authorMichaelidis, T. M.en
dc.contributor.authorSendtner, M.en
dc.contributor.authorCooper, J. D.en
dc.contributor.authorAiraksinen, M. S.en
dc.contributor.authorHoltmann, B.en
dc.contributor.authorMeyer, M.en
dc.contributor.authorThoenen, H.en
dc.date.accessioned2015-11-24T16:31:33Z
dc.date.available2015-11-24T16:31:33Z
dc.identifier.issn0896-6273-
dc.identifier.urihttps://olympias.lib.uoi.gr/jspui/handle/123456789/7458
dc.rightsDefault Licence-
dc.subjectneurotrophic factor preventsen
dc.subjectdeveloping nervous-systemen
dc.subjectprogrammed cell-deathen
dc.subjectmotor-neuronsen
dc.subjecttransgenic miceen
dc.subjectprotooncogene bcl-2en
dc.subjecttargeted disruptionen
dc.subjectsequence similarityen
dc.subjectprotein expressionen
dc.subjectlymphoid-tissuesen
dc.titleInactivation of bcl-2 results in progressive degeneration of motoneurons, sympathetic and sensory neurons during early postnatal developmenten
heal.abstractBcl-2 is a major regulator of programmed cell death, a critical process in shaping the developing nervous system. To assess whether Bcl-2 is involved in regulating neuronal survival and in mediating the neuroprotective action of neurotrophic factors, we generated Bcl-5-deficient mice. At birth, the number of facial motoneurons, sensory, and sympathetic neurons was not significantly changed, and axotomy-induced degeneration of facial motoneurons could still be prevented by brain-derived neurotrophic factor (BDNF) or ciliary neurotrophic factor (CNTF). Interestingly, substantial degeneration of motoneurons, sensory, and sympathetic neurons occurred after the physiological cell death period. Accordingly, Bcl-2 is not a permissive factor for the action of neurotrophic factors, and although it does not influence prenatal neuronal survival, it is crucial for the maintenance of specific populations of neurons during the early postnatal period.en
heal.accesscampus-
heal.fullTextAvailabilityTRUE-
heal.identifier.secondary<Go to ISI>://A1996UY98100009-
heal.journalNameNeuronen
heal.journalTypepeer reviewed-
heal.languageen-
heal.publicationDate1996-
heal.recordProviderΠανεπιστήμιο Ιωαννίνων. Σχολή Επιστημών και Τεχνολογιών. Τμήμα Βιολογικών Εφαρμογών και Τεχνολογιώνel
heal.typejournalArticle-
heal.type.elΆρθρο Περιοδικούel
heal.type.enJournal articleen

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