Genetic analysis of learning and memory deficits in senescence-accelerated mouse (SAM)

被引:5
作者
Tomobe, K
Isobe, M
Okuma, Y
Kitamura, K
Oketani, Y
Nomura, Y [1 ]
机构
[1] Hokkaido Univ, Grad Sch Pharmaceut Sci, Dept Pharmacol, Sapporo, Hokkaido 0600812, Japan
[2] Toyama Univ, Fac Engn, Dept Mat & Biosyst Engn, Mol & Cellular Biol Lab, Toyama 9308555, Japan
[3] New Drug Dev Res Ctr Inc, Eniwa 4521, Japan
关键词
senescence-accelerated mouse (SAM); learning and memory deficits; cross-mating; polygenic inheritance; passive avoidance;
D O I
10.1016/j.physbeh.2004.12.012
中图分类号
B84 [心理学];
学科分类号
04 ; 0402 ;
摘要
Genetic analysis of learning and memory deficits (LMD) in senescence-accelerated mouse P8 (SAMP8) was performed by cross-mating SAMP8 and Japanese Fancy Mouse 1 (JF1). The incidence of LMD in the F2 generation showed a 3:1 segregation ratio of mice with LMD to normal mice, and the incidence of LMD in the backcross generation of the F1 to JF1 parental strain was in agreement with a 1: 1 ratio of mice with LMD to normal mice. Estimation of the number of genes involved in the development of LMD using Wright's formula showed that at least two to four genes are involved. These results suggest that the inheritance of LMD is polygenically controlled and that there may be a single major gene, but this locus is not sex-linked. Moreover, hormonal influence on the development of LMD in SAMP8 females is of a genotype-dependent manner. (c) 2005 Elsevier Inc. All rights reserved.
引用
收藏
页码:505 / 510
页数:6
相关论文
共 31 条
  • [11] Estrous cycle influences the response of female rats in the elevated plus-maze test
    Marcondes, FK
    Miguel, KJ
    Melo, LL
    Spadari-Bratfisch, RC
    [J]. PHYSIOLOGY & BEHAVIOR, 2001, 74 (4-5) : 435 - 440
  • [12] Mather K., 1982, BIOMETRICAL GENETICS, V3rd
  • [13] AGE-RELATED-CHANGES IN LEARNING AND MEMORY IN THE SENESCENCE-ACCELERATED MOUSE (SAM)
    MIYAMOTO, M
    KIYOTA, Y
    YAMAZAKI, N
    NAGAOKA, A
    MATSUO, T
    NAGAWA, Y
    TAKEDA, T
    [J]. PHYSIOLOGY & BEHAVIOR, 1986, 38 (03) : 399 - 406
  • [14] The SAMP8 mouse: a model of Alzheimer disease?
    Morley, JE
    [J]. BIOGERONTOLOGY, 2002, 3 (1-2) : 57 - 60
  • [15] β-Amyloid precursor polypeptide in SAMP8 mice affects learning and memory
    Morley, JE
    Kumar, VB
    Bernardo, AE
    Farr, SA
    Uezu, K
    Tumosa, N
    Flood, JF
    [J]. PEPTIDES, 2000, 21 (12) : 1761 - 1767
  • [16] NOMURA Y, 1991, NMDA RECEPTOR RELATED AGENTS : BIOCHEMISTRY, PHARMACOLOGY AND BEHAVIOR, P287
  • [17] Alterations in acetylcholine, NMDA, benzodiazepine receptors and protein kinase C in the brain of the senescence-accelerated mouse: An animal model useful for studies on cognitive enhancers
    Nomura, Y
    Kitamura, Y
    Ohnuki, T
    Arima, T
    Yamanaka, Y
    Sasaki, K
    Oomura, Y
    [J]. BEHAVIOURAL BRAIN RESEARCH, 1997, 83 (1-2) : 51 - 55
  • [18] Do testosterone levels relate to aggression in elderly men with dementia?
    Orengo, C
    Kunik, ME
    Molinari, V
    Wristers, K
    Yudofsky, SC
    [J]. JOURNAL OF NEUROPSYCHIATRY AND CLINICAL NEUROSCIENCES, 2002, 14 (02) : 161 - 166
  • [19] ESTROGEN DEFICIENCY AND RISK OF ALZHEIMERS-DISEASE IN WOMEN
    PAGANINIHILL, A
    HENDERSON, VW
    [J]. AMERICAN JOURNAL OF EPIDEMIOLOGY, 1994, 140 (03) : 256 - 261
  • [20] Testosterone prevents the heat shock-induced overactivation of glycogen synthase kinase-3β but not of cyclin-dependent kinase 5 and c-Jun NH2-terminal kinase and concomitantly abolishes hyperphosphorylation of τ:: Implications of Alzheimer's disease
    Papasozomenos, SC
    Shanavas, A
    [J]. PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 2002, 99 (03) : 1140 - 1145