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Virus-mediated gene transfer into hippocampal CA1 region restores long-term potentiation in brain-derived neurotrophic factor mutant mice

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Korte,  M.
Theoretisches Teilinstitut Psychiatrie, MPI of Neurobiology, Max Planck Society;

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Griesbeck,  O.
Theoretisches Teilinstitut Psychiatrie, MPI of Neurobiology, Max Planck Society;

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Carroll,  P.
Theoretisches Teilinstitut Psychiatrie, MPI of Neurobiology, Max Planck Society;

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Staiger,  V.
Theoretisches Teilinstitut Psychiatrie, MPI of Neurobiology, Max Planck Society;

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Thoenen,  H.
Theoretisches Teilinstitut Psychiatrie, MPI of Neurobiology, Max Planck Society;

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Bonhoeffer,  Tobias
Theoretisches Teilinstitut Psychiatrie, MPI of Neurobiology, Max Planck Society;

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引用

Korte, M., Griesbeck, O., Gravel, C., Carroll, P., Staiger, V., Thoenen, H., & Bonhoeffer, T. (1996). Virus-mediated gene transfer into hippocampal CA1 region restores long-term potentiation in brain-derived neurotrophic factor mutant mice. Proceedings of the National Academy of Sciences of the United States of America, 93(22), 12547-12552. doi:10.1073/pnas.93.22.12547.


引用: https://hdl.handle.net/21.11116/0000-000B-3A46-6
要旨
Long-term potentiation (LTP) has been shown to be impaired in mice deficient in the brain-derived neurotrophic factor (BDNF) gene, as well as in a number of other knockout animals. Despite its power the gene-targeting approach is always fraught with the danger of looking at the cumulative direct and indirect effects of the absence of a particular gene rather than its immediate function. The re-expression of a specific gene at a selective time point and at a specific site in gene-defective mutants presents a potent procedure to overcome this limitation and to evaluate the causal relationship between the absence of a particular gene and the impairment of a function in gene-defective animals. Here we demonstrate that the re-expression of the BDNF gene in the CA1 region almost completely restores the severely impaired LTP in hippocampal slices of BDNF-deficient mice. The results therefore provide strong evidence for the direct involvement of BDNF in the process of LTP.