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Journal Article

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

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Borchardt,  Thilo
Department of Molecular Neurobiology, Max Planck Institute for Medical Research, Max Planck Society;

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Bus,  Thorsten
Max Planck Research Group Behavioural Neurophysiology (Andreas T. Schaefer), Max Planck Institute for Medical Research, Max Planck Society;

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

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Citation

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.


Cite as: http://hdl.handle.net/21.11116/0000-0002-E343-2
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.