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          Institute: MPI für medizinische Forschung     Collection: Abteilung Molekulare Neurobiologie     Display Documents



ID: 566782.0, MPI für medizinische Forschung / Abteilung Molekulare Neurobiologie
Excessive novelty−induced c−Fos expression and altered neurogenesis in the hippocampus of GluA1 knockout mice
Translation of Title:Excessive novelty−induced c−Fos expression and altered neurogenesis in the hippocampus of GluA1 knockout mice
Authors:Procaccini, Chiara; Aitta−aho, Teemu; Jaako−Movits, Külli; Zharkovsky, Alexander; Panhelainen, Anne; Sprengel, Rolf; Linden, Anni−Maija; Korpi, Esa R.
Language:English
Date of Publication (YYYY-MM-DD):2011-01-04
Title of Journal:European Journal of Neuroscience
Journal Abbrev.:Eur. J. Neurosci.
Volume:33
Issue / Number:1
Start Page:161
End Page:174
Review Status:Peer-review
Audience:Experts Only
Intended Educational Use:No
Abstract / Description: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
Free Keywords:AMPA receptors, BrdU, dentate gyrus, hyperlocomotion, immediate−early gene
Last Change of the Resource (YYYY-MM-DD):--
External Publication Status:published
Document Type:Article
Communicated by:Wulf Kaiser
Affiliations:MPI für medizinische Forschung/Abteilung Molekulare Neurobiologie
MPI für medizinische Forschung/Abteilung Zellphysiologie/Olfaction Web
MPI für medizinische Forschung/Abteilung Molekulare Neurobiologie/Gruppe Rolf Sprengel
Identifiers:LOCALID:7620
URI:http%3A%2F%2Fonlinelibrary.wiley.com%2Fdoi%2F10.11...
URI:http%3A%2F%2Fonlinelibrary.wiley.com%2Fdoi%2F10.11...
URI:http%3A%2F%2Fonlinelibrary.wiley.com%2Fdoi%2F10.11...
DOI:10.1111%2Fj.1460-9568.2010.07485.x
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