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

相关论文

共 26 条

[1] Uptake and pathogenic effects of amyloid beta peptide 1-42 are enhanced by integrin antagonists and blocked by NMDA receptor antagonists [J].

Bi, X ;

Gall, CM ;

Zhou, J ;

Lynch, G .

NEUROSCIENCE, 2002, 112 (04) :827-840

[2] Impaired synaptic plasticity and learning in aged amyloid precursor protein transgenic mice [J].

Chapman, PF ;

White, GL ;

Jones, MW ;

Cooper-Blacketer, D ;

Marshall, VJ ;

Irizarry, M ;

Younkin, L ;

Good, MA ;

Bliss, TVP ;

Hyman, BT ;

Younkin, SG ;

Hsiao, KK .

NATURE NEUROSCIENCE, 1999, 2 (03) :271-276

[3]

Chen QS, 2000, J NEUROSCI RES, V60, P65, DOI 10.1002/(SICI)1097-4547(20000401)60:1<65::AID-JNR7>3.0.CO

[4]

2-Q

[5] Alzheimer amyloid β-peptide inhibits the late phase of long-term potentiation through calcineurin-dependent mechanisms in the hippocampal dentate gyrus [J].

Chen, QS ;

Wei, WZ ;

Shimahara, T ;

Xie, CW .

NEUROBIOLOGY OF LEARNING AND MEMORY, 2002, 77 (03) :354-371

[6] Effects of beta-amyloid-(25-35) peptides on radioligand binding to excitatory amino acid receptors and voltage-dependent calcium channels: Evidence for a selective affinity for the glutamate and glycine recognition sites of the NMDA receptor [J].

Cowburn, RF ;

Wiehager, B ;

Trief, E ;

LiLi, M ;

Sundstrom, E .

NEUROCHEMICAL RESEARCH, 1997, 22 (12) :1437-1442

[7] Blockade of long-term potentiation by β-amyloid peptides in the CA1 region of the rat hippocampus in vivo [J].

Freir, DB ;

Holscher, C ;

Herron, CE .

JOURNAL OF NEUROPHYSIOLOGY, 2001, 85 (02) :708-713

[8] NEURODEGENERATION MEDIATED BY GLUTAMATE AND BETA-AMYLOID PEPTIDE - A COMPARISON AND POSSIBLE INTERACTION [J].

GRAY, CW ;

PATEL, AJ .

BRAIN RESEARCH, 1995, 691 (1-2) :169-179

[9] β-Amyloid neurotoxicity is mediated by a glutamate-triggered excitotoxic cascade in rat nucleus basalis [J].

Harkany, T ;

Abrahám, I ;

Timmerman, W ;

Laskay, G ;

Tóth, B ;

Sasvári, M ;

Kónya, C ;

Sebens, JB ;

Korf, J ;

Nyakas, C ;

Zarándi, M ;

Soós, K ;

Penke, B ;

Luiten, PGM .

EUROPEAN JOURNAL OF NEUROSCIENCE, 2000, 12 (08) :2735-2745

[10] Pentapeptide amides interfere with the aggregation of β-amyloid peptide of Alzheimer's disease [J].

Hetényi, C ;

Szabó, Z ;

Klement, T ;

Datki, Z ;

Körtvélyesi, T ;

Zarándi, M ;

Penke, B .

BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, 2002, 292 (04) :931-936