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  Somatic accumulation of GluA1-AMPA receptors leads to selective cognitive impairments in mice

Bannerman, D. M., Borchardt, T., Jensen, V., Rozov, A., Haj-Yasein, N. N., Burnashev, N., et al. (2018). Somatic accumulation of GluA1-AMPA receptors leads to selective cognitive impairments in mice. Frontiers in Molecular Neuroscience, 2018(11): 199, pp. 1-14. doi:10.3389/fnmol.2018.00199.

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Item Permalink: http://hdl.handle.net/21.11116/0000-0002-E343-2 Version Permalink: http://hdl.handle.net/21.11116/0000-0002-E544-F
Genre: Journal Article

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FrontMolNeurosci_11_2018_199.pdf (Any fulltext), 4MB
 
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 Creators:
Bannerman, David M., Author
Borchardt, Thilo1, Author              
Jensen, Vidar, Author
Rozov, Andrey, Author
Haj-Yasein, Nadia N., Author
Burnashev, Nail, Author
Zamanillo, Daniel, Author
Bus, Thorsten2, Author              
Grube, Isabel, Author
Adelmann, Giselind, Author
Rawlins, J. Nicholas P., Author
Sprengel, Rolf1, Author              
Affiliations:
1Department of Molecular Neurobiology, Max Planck Institute for Medical Research, Max Planck Society, ou_1497704              
2Max Planck Research Group Behavioural Neurophysiology (Andreas T. Schaefer), Max Planck Institute for Medical Research, Max Planck Society, ou_1497722              

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Free keywords: AMPA receptors; GluA1; Morris water-maze; RNA-editing; long-term potentiation; spatial memory; spatial working memory
 Abstract: The GluA1 subunit of the L-α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptor (AMPAR) plays a crucial, but highly selective, role in cognitive function. Here we analyzed AMPAR expression, AMPAR distribution and spatial learning in mice (Gria1R/R ), expressing the "trafficking compromised" GluA1(Q600R) point mutation. Our analysis revealed somatic accumulation and reduction of GluA1(Q600R) and GluA2, but only slightly reduced CA1 synaptic localization in hippocampi of adult Gria1R/R mice. These immunohistological changes were accompanied by a strong reduction of somatic AMPAR currents in CA1, and a reduction of plasticity (short-term and long-term potentiation, STP and LTP, respectively) in the CA1 subfield following tetanic and theta-burst stimulation. Nevertheless, spatial reference memory acquisition in the Morris water-maze and on an appetitive Y-maze task was unaffected in Gria1R/R mice. In contrast, spatial working/short-term memory during both spontaneous and rewarded alternation tasks was dramatically impaired. These findings identify the GluA1(Q600R) mutation as a loss of function mutation that provides independent evidence for the selective role of GluA1 in the expression of short-term memory.

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Language(s): eng - English
 Dates: 2018-02-072018-05-182018-06-25
 Publication Status: Published online
 Pages: 14
 Publishing info: -
 Table of Contents: -
 Rev. Method: Peer
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Title: Frontiers in Molecular Neuroscience
Source Genre: Journal
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Publ. Info: Lausanne, Switzerland : Frontiers Research Foundation
Pages: - Volume / Issue: 2018 (11) Sequence Number: 199 Start / End Page: 1 - 14 Identifier: ISSN: 1662-5099
CoNE: https://pure.mpg.de/cone/journals/resource/1662-5099