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Mice with a fra-1 knock-in into the c-fos locus show impaired spatial but regular contextual learning and normal LTP

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Sprengel,  Rolf
Department of Molecular Neurobiology, Max Planck Institute for Medical Research, Max Planck Society;

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Citation

Gass, P., Fleischmann, A., Hvalby, Ø., Jensen, V., Zacher, C., Strekalova, T., et al. (2004). Mice with a fra-1 knock-in into the c-fos locus show impaired spatial but regular contextual learning and normal LTP. Molecular Brain Research, 130(1), 16-22. doi:10.1016/j.molbrainres.2004.07.004.


Cite as: http://hdl.handle.net/11858/00-001M-0000-002A-18A0-3
Abstract
The immediate early gene c-fos is part of the AP-1 transcription factor complex, which is involved in molecular mechanisms underlying learning and memory. Mice that lack c-Fos in the brain show impairments in spatial reference and contextual learning, and also exhibit a reduced long-term potentiation of synaptic transmission (LTP) at CA3-to-CA1 synapses. In the present study, we investigated mice in which c-fos was deleted and replaced by fra-1 (c-fos(fra-1) mice) to determine whether other members of the c-fos gene family can substitute for the functions of the c-fos gene. In c-fos(fra-1) mice, both CA3-to-CA1 LTP and contextual learning in a Pavlovian fear conditioning task were similar to wild-type littermates, indicating that Fra-1 expression restored the impairments caused by brain-specific c-Fos depletion. However, c-Fos-mediated learning deficits in a reference memory task of the Morris watermaze were also present in c-fos(fra-1) mice. These findings suggest that different c-Fos target genes are involved in LTP, contextual learning, and spatial reference memory formation.