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N–(p–amylcinnamoyl) anthranilic acid attenuates remedial effects of memantine on memory deficits following intracerebroventricular streptozotocin administration in rats

M. Göl, Ş. Demiryürek, D. S. Kaplan, A. Saracaloğlu, M. Örkmez, A. T. Demiryürek


N–(p–amylcinnamoyl) anthranilic acid (ACA) is a blocker of transient receptor potential melastatin–2 (TRPM2) which is a non–selective, Ca2+–permeable cation channel. The purpose of this study was to investigate effects of ACA on a rat model of streptozotocin (STZ)–induced learning and memory deficits. A total of 60 Wistar rats randomly divided into six groups; (1) control, (2) sham–operated, (3) intracerebroventricular STZ (ICV–STZ) administered, (4) ICV–STZ + memantine (5 mg/kg i.p.), (5) ICV–STZ + ACA (25 mg/kg i.p.) and (6) ICV–STZ + ACA (25 mg/kg) + memantine (5 mg/kg). Memantine treatment ameliorated the spatial memory deficits induced by ICV–STZ administration. However, ACA treatment did not provide any improvement, instead positive effects of memantine on learning and memory deficits were attenuated by ACA treatment. Western blot analysis in hippocampal tissues showed that TRPM2–L protein expression was markedly suppressed in ICV–STZ administered group. The ACA treatment reversed that suppression. Surprisingly, the memantine treatment resulted in overexpression of TRPM2–L, to a certain extent. In conclusion, our findings showed for the first time that TRPM2–L protein expression was significantly suppressed in the ICV–STZ induced memory impairment model. Even though ACA reversed this suppression, no improvement in spatial memory was observed following ACA treatment.


N–(p–amylcinnamoyl) anthranilic acid; TRPM2 channels, memantine.

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