M. Bannerman, David Borchardt, Thilo Jensen, Vidar Rozov, Andrey Haj-Yasein, Nadia N. Burnashev, Nail Zamanillo, Daniel Bus, Thorsten Grube, Isabel Adelmann, Giselind Rawlins, J. Nicholas P. Sprengel, Rolf Data_Sheet_1_Somatic Accumulation of GluA1-AMPA Receptors Leads to Selective Cognitive Impairments in Mice.DOCX <p>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 (Gria1<sup>R/R</sup>), 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 Gria1<sup>R/R</sup> 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 Gria1<sup>R/R</sup> 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.</p> AMPA receptors;GluA1;long-term potentiation;Morris water-maze;RNA-editing;spatial memory;spatial working memory 2018-06-25
    https://frontiersin.figshare.com/articles/dataset/Data_Sheet_1_Somatic_Accumulation_of_GluA1-AMPA_Receptors_Leads_to_Selective_Cognitive_Impairments_in_Mice_DOCX/6667880
10.3389/fnmol.2018.00199.s001