Enhancement of NMDA responses by β-amyloid peptides in the hippocampus in vivo

被引：55
作者：
Molnár, Z
Soós, K
Lengyel, I
Penke, B
Szegedi, V
Budai, D
机构：
[1] Univ Szeged, Juhasz Gyula Coll, Dept Biol, H-6721 Szeged, Hungary
[2] Univ Szeged, Juhasz Gyula Coll, Dept Med Chem, H-6721 Szeged, Hungary
[3] Hungarian Acad Sci, Biol Res Ctr, Dept Biochem, H-6701 Szeged, Hungary
[4] Hungarian Acad Sci, Prot Res Grp, H-6701 Szeged, Hungary
来源：
NEUROREPORT | 2004年 / 15卷 / 10期
关键词：
Alzheimer's disease; amyloid beta-peptide; amyloid fragment; microiontophoresis; NMDA; rat; single-unit recording;
D O I：
10.1097/01.wnr.0000134471.06244.d2
中图分类号：
Q189 [神经科学];
学科分类号：
071006 ;
摘要：
The effects of Alzheimer's disease-related beta-amyloid (AD) peptides on the N-methyl-D-aspartate (NMDA)-evoked cell firing rate were studied in hippocampal CA1 neurons of the rat. Extracellular single-unit recordings were combined with iontophoretic applications that allowed quantitative analyses of the interactions between AD peptides and NMDA receptor-mediated events in vivo. The NMDA responses were significantly increased both by the full length Abeta1-42 and by its model fragment Abeta25-35. Enhancements of the NMDA responses by the AD peptides lasted about 15 min and were irreversible. The effects of Abeta25-35 were prevented by the pentapeptide Lys-Leu-Val-Gly-Phe-amide (KLVGF) and were not evoked when its reversed sequence (Abeta35-25) was applied.
引用
收藏
页码：1649 / 1652
页数：4
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