Emotional disorders and memory deficits in senescence-accelerated mice, SAMP8 and SAMP10

被引:2
作者
Miyamoto, M [1 ]
机构
[1] Takeda Chem Ind Ltd, Pharmaceut Res Div, Pharmacol Res Labs 2, Tsukuba, Ibaraki 3004293, Japan
来源
SENESCENCE-ACCELERATED MOUSE (SAM): AN ANIMAL MODEL OF SENESCENCE | 2004年 / 1260卷
关键词
senescence; accelerated mouse; SAMP8; SAMP10; learning and memory; emotional behavior; anxiety; behavioral depression; circadian rhythm; oxidative stress;
D O I
10.1016/S0531-5131(03)01597-8
中图分类号
R592 [老年病学]; C [社会科学总论];
学科分类号
03 ; 0303 ; 100203 ;
摘要
The senescence-accelerated mouse (SAMP8) showed age-related deficits in avoidance and spatial teaming tasks, and also exhibited reduced anxiety-like behavior in tests involving food neophobia, an elevated plus-maze and punished water-licking. The emotional change in SAMP8 was considered to be closely related to the deficits in the teaming tasks. Aged SAMR1 showed similar behavioral changes to those in SAMP8 mice, indicating that some of the behavioral changes in SAMP8 may be derived from accelerated aging. SAMP10 mice also showed teaming impairment in the avoidance tasks, although the impairment was less than that in SAMP8 mice. SAMP10 exhibited marked behavioral depression when subjected to a tail suspension test or forced swimming test. Thus, the SAMP 10 strain may be useful for studying age-related behavioral depression and reduced spontaneity. SAMP8 and SAMP10 also exhibited marked disruption of the circadian rhythms of spontaneous motor activity (SMA) and drinking behavior, and bright light stimulation ameliorated the abnormal circadian rhythms in SAMP8. These findings suggest that SAMP8 and SAMP10 are also valid animal models for age-related disorders of learning and memory, emotional behavior and circadian rhythms in elderly humans and in those with senile dementia. (C) 2003 Elsevier B.V. All rights reserved.
引用
收藏
页码:99 / 106
页数:8
相关论文
共 36 条
[1]   AGING, ENERGY, AND OXIDATIVE STRESS IN NEURODEGENERATIVE DISEASES [J].
BEAL, MF .
ANNALS OF NEUROLOGY, 1995, 38 (03) :357-366
[2]   Free radical oxidation of brain proteins in accelerated senescence and its modulation by N-tert-butyl-alpha-phenylnitrone [J].
Butterfield, DA ;
Howard, BJ ;
Yatin, S ;
Allen, KL ;
Carney, JM .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1997, 94 (02) :674-678
[3]  
COLWELL CS, 1993, J NEUROSCI, V13, P1454
[4]   THE SPIN-TRAP N-TERT-ALPHA-PHENYL-BUTYLNITRONE PROLONGS THE LIFE-SPAN OF THE SENESCENCE-ACCELERATED MOUSE [J].
EDAMATSU, R ;
MORI, A ;
PACKER, L .
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, 1995, 211 (03) :847-849
[5]   AGE-RELATED-CHANGES IN FOOTSHOCK AVOIDANCE ACQUISITION AND RETENTION IN SENESCENCE ACCELERATED MOUSE (SAM) [J].
FLOOD, JF ;
MORLEY, JE .
NEUROBIOLOGY OF AGING, 1993, 14 (02) :153-157
[6]   Increased mitochondrial DNA deletion in the brain of SAMP8, a mouse model for spontaneous oxidative stress brain [J].
Fujibayashi, Y ;
Yamamoto, S ;
Waki, A ;
Konishi, J ;
Yonekura, Y .
NEUROSCIENCE LETTERS, 1998, 254 (02) :109-112
[7]   Involvement of the glutamatergic system in behavioral disorders in senescence-accelerated mice (SAMP8) [J].
Fujiwara, Y ;
Takahashi, H ;
Hirai, K ;
Miyamoto, M .
SENESCENCE-ACCELERATED MOUSE (SAM): AN ANIMAL MODEL OF SENESCENCE, 2004, 1260 :303-308
[8]   FREE-RADICAL THEORY OF AGING - INCREASING THE FUNCTIONAL LIFE-SPAN [J].
HARMAN, D .
PHARMACOLOGY OF AGING PROCESSES: METHODS OF ASSESSMENT AND POTENTIAL INTERVENTIONS, 1994, 717 :1-15
[9]   EFFECTS OF AGE AND STRESS ON REGIONAL NORADRENALINE METABOLISM IN THE RAT-BRAIN [J].
IDA, Y ;
TANAKA, M ;
KOHNO, Y ;
NAKAGAWA, R ;
IIMORI, K ;
TSUDA, A ;
HOAKI, Y ;
NAGASAKI, N .
NEUROBIOLOGY OF AGING, 1982, 3 (03) :233-236
[10]   CIRCADIAN RHYTHMICITY AND SLEEP - EFFECTS OF AGING IN LABORATORY-ANIMALS [J].
INGRAM, DK ;
LONDON, ED ;
REYNOLDS, MA .
NEUROBIOLOGY OF AGING, 1982, 3 (04) :287-297