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pubmed-article:15236231pubmed:abstractTextThe number of cerebellar Purkinje cells is increased by over 40% in young transgenic mice that overexpress a human Bcl-2 transgene (Hu-Bcl-2). To determine whether the Bcl-2-mediated rescue of Purkinje cells persists through life, the numbers of Purkinje cells were estimated in 6-, 12-, 18-, and 24-month-old Hu-Bcl-2 transgenic mice and age-matched controls. In addition, the expression of four markers for Purkinje cell differentiation, calbindin (CaBP), the 67-kDa isoform of glutamic acid decarboxylase (GAD67), gamma-aminobutyric acid transaminase (GABA-T), and the NMDA-R1 receptor subtype (NMDA-NR1) was analyzed in 6-month-old Hu-Bcl-2 transgenics and controls to determine whether overexpression of Bcl-2 and rescue from naturally occurring cell death affects the normal differentiation of Purkinje cells. The estimates of Purkinje cell numbers showed that the number of Purkinje cells in the Hu-Bcl-2 transgenics declines after 6 months to approach wild-type values by 18 months. Although the exogenous human BCL-2 is still expressed in Purkinje cells at 24 months, the expression levels of human BCL-2 appear to decline significantly after 6 months, suggesting that survival of the supernumary Purkinje cells depends on the sustained overexpression of Bcl-2. All the Purkinje cells in the Hu-Bcl-2 transgenic mice appeared to express normal levels of the differentiation markers analyzed so there was no evidence for a class of Purkinje cells that do not differentiate normally when rescued from naturally occurring cell death.lld:pubmed
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pubmed-article:15236231pubmed:copyrightInfoCopyright 2004 Wiley-Liss, Inc.lld:pubmed
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pubmed-article:15236231pubmed:articleTitleCerebellar Purkinje cell loss in aging Hu-Bcl-2 transgenic mice.lld:pubmed
pubmed-article:15236231pubmed:affiliationLab. Développement et Vieillissement du Système Nerveux (DVSN), UMR NPA 7102 Centre National de la Recherche Scientifique and Université Pierre and Marie Curie, 75005 Paris, France.lld:pubmed
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pubmed-article:15236231pubmed:publicationTypeResearch Support, U.S. Gov't, P.H.S.lld:pubmed
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