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Glutamate neurotransmission stands as an important issue to minimize memory impairment. We investigated the effects of an inhibitor of α-amino-3-hydroxy-5-methyl-4-isozazole propionic acid receptors (AMPA) endocytosis and GluN2B subunit of N-methyl-d-aspartate receptors (NMDA), either isolated or combined, on memory impairments induced by Amyloid beta1-42 (Aβ). Eighty male Wistar rats were used for two experiments of consolidation and retrieval of memory. Memory impairment was induced by intracerebroventricular (ICV) injection of Aβ1-42 (2 μg/μl), and evaluated using Morris Water Maze (MWM). Each experiment consisted of 5 groups: Saline + Saline, Aβ + Saline, Aβ + Ifenprodil (Ifen, 3 nmol/ICV), Aβ +Tat-GluR23Y (3 µmol/kg/IP), and Aβ1 +Ifen + Tat-GluR23Y. Then, hippocampal cAMP-response element-binding protein (CREB) was measured by western blotting. Data were analyzed by Analysis of variance (ANOVA) repeated measure, and one-way Anova followed by Tukey’s post hoc test. During retrieval, Aβ+ Tat-GluR23Y showed significant improvement in total time spent (TTS) in the target quadrant ( p  = 0.009), escape latency to a platform ( p  = 0.008) and hippocampal level of CREB ( p  = 0.006) compared with Aβ + saline. Also, coadministration of Tat-GluR23Yand Ifen similar to Tat-GluR23Y alone caused significant improvement in TTS ( p  = 0.014) and latency to platform ( p  = 0.013). During consolidation, shorter escape latency ( p  = 0.001), longer TTS ( p  = 0.002) and higher level of hippocampal CREB were observed in the Aβ + Tat-GluR23Y ( p  = 0.001) and Aβ+ Tat-GluR23Y + Ifen ( p  = 0.017), respectively. The present study provides pieces of evidence that inhibition of AMPARs endocytosis using Tat-GluR23Y facilitates memory consolidation and retrieval in  A β induced memory impairment  via  the CREB signaling pathway.

Co-treatment of AMPA endocytosis inhibitor and GluN2B antagonist facilitate consolidation and retrieval of memory impaired by β amyloid peptide