Mouse models for psychiatric disorders

被引:65
作者
Seong, E
Seasholtz, AF
Burmeister, M
机构
[1] Univ Michigan, Mental Hlth Res Inst, Program Neurosci, Ann Arbor, MI 48109 USA
[2] Univ Michigan, Mental Hlth Res Inst, Dept Biol Chem, Ann Arbor, MI 48109 USA
[3] Univ Michigan, Mental Hlth Res Inst, Dept Human Genet & Psychiat, Ann Arbor, MI 48109 USA
关键词
D O I
10.1016/S0168-9525(02)02807-X
中图分类号
Q3 [遗传学];
学科分类号
071007 ; 090102 ;
摘要
Genes involved in psychiatric disorders are difficult to identify, and those that have been proposed so far remain ambiguous. As it is unrealistic to expect the development of, say, a 'schizophrenic' or 'autistic' mouse, mice are unlikely to have the same role in gene identification in psychiatry as circling mice did in the discovery of human deafness genes. However, many psychiatric disorders are associated with intermediate phenotypes that can be modeled and studied in mice, including physiological or anatomical brain changes and behavioral traits. Mouse models help to evaluate the effect of a human candidate gene mutation on an intermediate trait, and to identify new candidate genes. Once a gene or pathway has been identified, mice are also used to study the interplay of different genes in that system.
引用
收藏
页码:643 / 650
页数:8
相关论文
共 75 条
[1]   A targeted mutation of the D-3 dopamine receptor gene is associated with hyperactivity in mice [J].
Accili, D ;
Fishburn, CS ;
Drago, J ;
Steiner, H ;
Lachowicz, JE ;
Park, BH ;
Gauda, EB ;
Lee, EJ ;
Cool, MH ;
Sibley, DR ;
Gerfen, CR ;
Westphal, H ;
Fuchs, S .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1996, 93 (05) :1945-1949
[2]   Identification of DNA variants in the SNAP-25 gene and linkage study of these polymorphisms and attention-deficit hyperactivity disorder [J].
Barr, CL ;
Feng, Y ;
Wigg, K ;
Bloom, S ;
Roberts, W ;
Malone, M ;
Schachar, R ;
Tannock, R ;
Kennedy, JL .
MOLECULAR PSYCHIATRY, 2000, 5 (04) :405-409
[3]  
BARRETT TB, IN PRESS MOL PSYCHIA
[4]   Association between-G308A tumor necrosis factor alpha gene polymorphism and schizophrenia [J].
Boin, F ;
Zanardini, R ;
Pioli, R ;
Altamura, CA ;
Maes, M ;
Gennarelli, M .
MOLECULAR PSYCHIATRY, 2001, 6 (01) :79-82
[5]   ABNORMAL-BEHAVIOR ASSOCIATED WITH A POINT MUTATION IN THE STRUCTURAL GENE FOR MONOAMINE OXIDASE-A [J].
BRUNNER, HG ;
NELEN, M ;
BREAKEFIELD, XO ;
ROPERS, HH ;
VANOOST, BA .
SCIENCE, 1993, 262 (5133) :578-580
[6]   The mouse: Genetics meets behaviour [J].
Bucan, M ;
Abel, T .
NATURE REVIEWS GENETICS, 2002, 3 (02) :114-123
[7]   AGGRESSIVE-BEHAVIOR AND ALTERED AMOUNTS OF BRAIN-SEROTONIN AND NOREPINEPHRINE IN MICE LACKING MAOA [J].
CASES, O ;
SEIF, I ;
GRIMSBY, J ;
GASPAR, P ;
CHEN, K ;
POURNIN, S ;
MULLER, U ;
AGUET, M ;
BABINET, C ;
SHIH, JC ;
DEMAEYER, E .
SCIENCE, 1995, 268 (5218) :1763-1766
[8]   Genotype-based screen for ENU-induced mutations in mouse embryonic stem cells [J].
Chen, YJ ;
Yee, D ;
Dains, K ;
Chatterjee, A ;
Cavalcoli, J ;
Schneider, E ;
Om, J ;
Woychik, RP ;
Magnuson, T .
NATURE GENETICS, 2000, 24 (03) :314-317
[9]   A gene-driven approach to the identification of ENU mutants in the mouse [J].
Coghill, EL ;
Hugill, A ;
Parkinson, N ;
Davison, C ;
Glenister, P ;
Clements, S ;
Hunter, J ;
Cox, RD ;
Brown, SDM .
NATURE GENETICS, 2002, 30 (03) :255-256
[10]  
COOK EH, 1995, AM J HUM GENET, V56, P993