Single intracerebroventricular administration of amyloid-beta (25-35) peptide induces impairment in short-term rather than long-term memory in rats

被引:97
作者
Stepanichev, MY [1 ]
Moiseeva, YV [1 ]
Lazareva, NA [1 ]
Onufriev, MV [1 ]
Gulyaeva, NV [1 ]
机构
[1] Russian Acad Sci, Inst Higher Nervous Activ & Neurophysiol, Dept Funct Biochem Nervous Syst, Moscow 117485, Russia
基金
俄罗斯基础研究基金会;
关键词
amyloid-beta (25-35) peptide; short-term memory; working memory; long-term memory; 8-arm radial maze; Y-maze; passive avoidance; social recognition;
D O I
10.1016/S0361-9230(03)00118-7
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
Ample experimental evidence indicates that intracerebral injection or infusion of amyloid-beta peptides (Abeta) to rodents induces learning and memory impairments as well as neurodegeneration in brain areas related to cognitive function. In the present study, we assessed the effects of a single intracerebroventricular (i.c.v.) injection of aggregated Abeta fragment (25-35) at a dose of 15 nmol/rat on short-term and long-term memory in rats during the 6-month post-surgery period. The results demonstrate that Abeta(25-35)-induced memory impairments in spontaneous alternation behavior in a Y-maze at 17, 36, and 180 days after the surgery as well as in a social recognition task 110 days post-surgery. Abeta(25-35) also impaired spatial memory in an 8-arm radial maze, but did not influence performance of the step-down passive avoidance task. These results suggest that Abeta(25-35) preferably induces impairments of spatial and non-spatial short-term (working) memory rather than long-term memory in rats. (C) 2003 Elsevier Science Inc. All rights reserved.
引用
收藏
页码:197 / 205
页数:9
相关论文
共 57 条
[1]   ADMINISTRATION OF AMYLOID BETA-PEPTIDES INTO THE MEDIAL SEPTUM OF RATS DECREASES ACETYLCHOLINE-RELEASE FROM HIPPOCAMPUS IN-VIVO [J].
ABE, E ;
CASAMENTI, F ;
GIOVANNELLI, L ;
SCALI, C ;
PEPEU, G .
BRAIN RESEARCH, 1994, 636 (01) :162-164
[2]   The mean A beta load in the hippocampus correlates with duration and severity of dementia in subgroups of Alzheimer disease [J].
Bartoo, GT ;
Nochlin, D ;
Chang, DY ;
Kim, Y ;
Sumi, SM .
JOURNAL OF NEUROPATHOLOGY AND EXPERIMENTAL NEUROLOGY, 1997, 56 (05) :531-540
[3]   ALTERED SYNAPTIC PLASTICITY AND MEMORY FORMATION IN NITRIC-OXIDE SYNTHASE INHIBITOR-TREATED RATS [J].
BOHME, GA ;
BON, C ;
LEMAIRE, M ;
REIBAUD, M ;
PIOT, O ;
STUTZMANN, JM ;
DOBLE, A ;
BLANCHARD, JC .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1993, 90 (19) :9191-9194
[4]   NEUROPATHOLOGICAL STAGING OF ALZHEIMER-RELATED CHANGES [J].
BRAAK, H ;
BRAAK, E .
ACTA NEUROPATHOLOGICA, 1991, 82 (04) :239-259
[5]  
BURES J., 1983, TECHNIQUES BASIC EXP
[6]   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
[7]   The neurochemical and behavioral effects of beta-amyloid peptide(25-35) [J].
Chen, SY ;
Wright, JW ;
Barnes, CD .
BRAIN RESEARCH, 1996, 720 (1-2) :54-60
[8]   Neuropathology of synthetic beta-amyloid peptide analogs in vivo [J].
Chen, SY ;
Harding, JW ;
Barnes, CD .
BRAIN RESEARCH, 1996, 715 (1-2) :44-50
[9]   AF64A-INDUCED WORKING MEMORY IMPAIRMENT - BEHAVIORAL, NEUROCHEMICAL AND HISTOLOGICAL CORRELATES [J].
CHROBAK, JJ ;
HANIN, I ;
SCHMECHEL, DE ;
WALSH, TJ .
BRAIN RESEARCH, 1988, 463 (01) :107-117
[10]   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