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  Excessive novelty-induced c-Fos expression and altered neurogenesis in the hippocampus of GluA1 knockout mice

Procaccini, C., Aitta-aho, T., Jaako-Movits, K., Zharkovsky, A., Panhelainen, A., Sprengel, R., et al. (2011). Excessive novelty-induced c-Fos expression and altered neurogenesis in the hippocampus of GluA1 knockout mice. European Journal of Neuroscience: European Neuroscience Association, 33(1), 161-174. doi:10.1111/j.1460-9568.2010.07485.x.

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Genre: Journal Article
Alternative Title : Excessive novelty-induced c-Fos expression and altered neurogenesis in the hippocampus of GluA1 knockout mice

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EurJNeurosci_33_2011_161.pdf (Any fulltext), 641KB
 
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 Creators:
Procaccini, Chiara, Author
Aitta-aho, Teemu, Author
Jaako-Movits, Külli, Author
Zharkovsky, Alexander, Author
Panhelainen, Anne, Author
Sprengel, Rolf1, Author           
Linden, Anni-Maija, Author
Korpi, Esa R., Author
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1Department of Molecular Neurobiology, Max Planck Institute for Medical Research, Max Planck Society, ou_1497704              

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Free keywords: AMPA receptors, BrdU, dentate gyrus, hyperlocomotion, immediate−early gene
 Abstract: a−Amino−3−hydroxy−5−methyl−4−isoxazolepropionic acid (AMPA) receptor GluA1 subunit−deficient (GluA1) / )) mice display noveltyinduced hyperactivity, cognitive and social defects and may model psychiatric disorders, such as schizophrenia and depression / mania. We used c−Fos expression in GluA1) / ) mice to identify brain regions responsible for novelty−induced hyperlocomotion. Exposure to a novel cage for 2 h significantly increased c−Fos expression in many brain regions in both wild−type and knockout mice. Interestingly, the clearest genotype effect was observed in the hippocampus and its main input region, the entorhinal cortex, where the novelty−induced c−Fos expression was more strongly enhanced in GluA1) / ) mice. Their novelty−induced hyperlocomotion partly depended on the activity of AMPA receptors, as it was diminished by the AMPA receptor antagonist 2,3−dioxo−6−nitro−1,2,3,4− tetrahydrobenzo[f]quinoxaline−7−sulphonamide (NBQX) and unaffected by the AMPA receptor potentiator 2,3−dihydro−1,4−benzodioxin− 6−yl−1−piperidinylmethanone (CX546). The hyperlocomotion of GluA1) / ) mice was normalised to the level of wild−type mice within 5−6 h, after which their locomotion followed normal circadian rhythm and was not affected by acute or chronic treatments with the selective serotonin reuptake inhibitor escitalopram. We propose that hippocampal dysfunction, as evidenced by the excessive c− Fos response to novelty, is the major contributor to novelty−induced hyperlocomotion in GluA1) / ) mice. Hippocampal dysfunction was also indicated by changes in proliferation and survival of adult−born dentate gyrus cells in the knockout mice. These results suggest focusing on the functions of hippocampal formation, such as novelty detection, when using the GluA1) / ) mouse line as a model for neuropsychiatric and cognitive disorders

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Language(s): eng - English
 Dates: 2010-09-212010-06-092010-09-242010-11-142011-01-04
 Publication Status: Issued
 Pages: 14
 Publishing info: -
 Table of Contents: -
 Rev. Type: Peer
 Degree: -

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Title: European Journal of Neuroscience : European Neuroscience Association
  Other : Eur. J. Neurosci
Source Genre: Journal
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Publ. Info: Oxford, UK : Published on behalf of the European Neuroscience Association by Oxford University Press
Pages: - Volume / Issue: 33 (1) Sequence Number: - Start / End Page: 161 - 174 Identifier: ISSN: 0953-816X
CoNE: https://pure.mpg.de/cone/journals/resource/954925575988