Attention-deficit hyperactivity disorder and the adrenergic receptors α1C and α2C

被引:38
作者
Barr, CL
Wigg, K
Zai, G
Roberts, W
Malone, M
Schachar, R
Tannock, R
Kennedy, JL
机构
[1] Toronto Western Hosp, Dept Psychiat, Toronto, ON M5T 2S8, Canada
[2] Hosp Sick Children, Dept Psychiat, Toronto, ON M5G 1X8, Canada
[3] Hosp Sick Children, Dept Paediat, Div Neurol, Toronto, ON M5G 1X8, Canada
[4] Univ Toronto, Clarke Div, Ctr Addict & Mental Hlth, Toronto, ON, Canada
基金
加拿大健康研究院;
关键词
attention-deficit hyperactivity disorder; adrenergic receptor alpha 1C; adrenergic receptor alpha 2C; linkage; norepinephrine;
D O I
10.1038/sj.mp.4000863
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
The adrenergic system has been hypothesized to be involved in the etiology of attention-deficit hyperactivity disorder (ADHD) based on pharmacological interventions and animal models. Noradrenergic neurons are implicated in the modulation of vigilance, improvement of visual attention, initiation of adaptive response, learning and memory. In this study we tested the genes for two adrenergic receptors, alpha 1C (ADRA1C) located on chromosome 8p11.2, and alpha 2C (ADRA2C) located on chromosome 4p16, as genetic susceptibility factors in ADHD. For the adrenergic receptor alpha 1C we used a C to T polymorphism that results in a change of Cys to Arg at codon 492 for the linkage study. For the adrenergic receptor alpha 2C gene we examined a dinucleotide repeat polymorphism located approximately 6 kb from the gene. We examined these polymorphisms in a sample of 103 families ascertained through an ADHD proband. Using the transmission disequilibrium test, we did not observe biased transmission of any of the alleles of these polymorphisms. We conclude that the alleles at the polymorphisms tested in these two genes are not linked to the ADHD phenotype in this sample of families.
引用
收藏
页码:334 / 337
页数:4
相关论文
共 29 条
[1]  
Arnsten AFT, 1996, ARCH GEN PSYCHIAT, V53, P448
[2]   Attention-deficit hyperactivity disorder and the gene for the dopamine D5 receptor [J].
Barr, CL ;
Wigg, KG ;
Feng, Y ;
Zai, G ;
Malone, M ;
Roberts, W ;
Schachar, R ;
Tannock, R ;
Kennedy, JL .
MOLECULAR PSYCHIATRY, 2000, 5 (05) :548-551
[3]  
Barr CL, 1999, AM J MED GENET, V88, P710, DOI 10.1002/(SICI)1096-8628(19991215)88:6<710::AID-AJMG23>3.0.CO
[4]  
2-Q
[5]   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
[6]  
Barr CL, 2000, AM J MED GENET, V96, P114
[7]  
BARR CL, IN PRESS BIOL PSYCHI
[8]   Attention-deficit/hyperactivity disorder (ADHD) as a noradrenergic disorder [J].
Biederman, J ;
Spencer, T .
BIOLOGICAL PSYCHIATRY, 1999, 46 (09) :1234-1242
[9]   EVALUATION OF THE REVISED ONTARIO CHILD HEALTH STUDY SCALES [J].
BOYLE, MH ;
OFFORD, DR ;
RACINE, Y ;
FLEMING, JE ;
SZATMARI, P ;
SANFORD, M .
JOURNAL OF CHILD PSYCHOLOGY AND PSYCHIATRY AND ALLIED DISCIPLINES, 1993, 34 (02) :189-213
[10]   Additive effect of three noradrenergic genes (ADRA2A, ADRA2C, DBH) on attention-deficit hyperactivity disorder and learning disabilities in Tourette syndrome subjects [J].
Comings, DE ;
Gade-Andavolu, R ;
Gonzalez, N ;
Blake, H ;
Wu, SJ ;
MacMurray, JP .
CLINICAL GENETICS, 1999, 55 (03) :160-172