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Increased generation of granule cells in adult Bcl-2-overexpressing mice: a role for cell death during continued hippocampal neurogenesis

Artikel i vetenskaplig tidskrift
Författare Hans-Georg Kuhn
Manfred Biebl
Daniel Wilhelm
Mingwei Li
Robert M. Friedlander
Jürgen Winkler
Publicerad i European Journal of Neuroscience
Volym 22
Nummer/häfte 8
Sidor 1907-1915
ISSN 0953-816X
Publiceringsår 2005
Publicerad vid Institutionen för klinisk neurovetenskap
Sidor 1907-1915
Språk en
Länkar dx.doi.org/10.1111/j.1460-9568.2005...
Ämnesord Animals, Apoptosis, genetics, Bromodeoxyuridine, metabolism, Cell Count, methods, Cell Differentiation, genetics, Cell Proliferation, Hippomane, cytology, physiology, Humans, Immunohistochemistry, methods, In Situ Nick-End Labeling, methods, Mice, Mice, Inbred C57BL, Mice, Transgenic, Microtubule-Associated Proteins, metabolism, Neurons, physiology, Neuropeptides, metabolism, Organogenesis, physiology, Phosphopyruvate Hydratase, metabolism, Proto-Oncogene Proteins c-bcl-2, genetics, physiology
Ämneskategorier Neurovetenskap

Sammanfattning

Programmed cell death is an important mechanism during brain development in order to control neuronal cell numbers and to correctly form neuronal circuitries. Programmed cell death is also present in neurogenic regions of the adult brain, and a significant portion of the adult-born cells is eliminated during the first months of maturation. We here address the question whether overexpression of the anti-apoptotic protein Bcl-2 would improve the survival of neural progenitor cells and, as a consequence, increase neurogenesis in the adult hippocampus. Transgenic animals, which express human Bcl-2 under the neuron-specific enolase promoter (NSE-huBcl-2), show a significant reduction of apoptotic cells in the hippocampal granule cell layer to about half of the wild-type level. These apoptotic cells are almost exclusively found in the zone of hippocampal progenitor activity and frequently co-label with the neuronal progenitor marker doublecortin (DCX). The rate of adult neurogenesis is doubled in the dentate gyrus of Bcl-2-overexpressing mice as demonstrated by quantification of progenitor cells using DCX and new neurons using bromodeoxyuridine (BrdU)/neuronal nuclei antigen (NeuN) double-labelling. The effect of Bcl-2 is limited to the late phase of progenitor maturation, as proliferation and early-phase progenitor cells were not affected. The increased level of neurogenesis leads to a significantly higher total number of granule cells in the dentate gyrus. These results underline the importance of developmental cell death during neurogenesis in the adult brain.

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