A Deletion in Tropomyosin-Related Kinase B and the Development of Human Anxiety

被引：20

作者：

Ernst, Carl ^{[1
]}

Wanner, Brigitte ^{[2
]}

Brezo, Jelena

Vitaro, Frank ^{[2
]}

Tremblay, Richard ^{[2
,3
]}

Turecki, Gustavo ^{[1
]}

机构：

[1] McGill Univ, Dept Psychiat, McGill Grp Suicide Studies, Verdun, PQ H4H 1R3, Canada

[2] Univ Montreal, Res Unit Childrens Psychosocial Maladjustment, Montreal, PQ, Canada

[3] Univ Coll Dublin, Sch Publ Hlth & Populat Sci, Dublin 2, Ireland

来源：

BIOLOGICAL PSYCHIATRY | 2011年 / 69卷 / 06期

基金：

加拿大自然科学与工程研究理事会;

关键词：

Brain; generalized anxiety disorder; genetics; longitudinal study; panic disorder; TrkB; TRKB NEUROTROPHIN RECEPTOR; BEHAVIOR; GENE; DISORDERS; STRESS; BDNF;

D O I：

10.1016/j.biopsych.2010.10.008

中图分类号：

Q189 [神经科学];

学科分类号：

071006 [神经生物学];

摘要：

Background: The tropomyosin-related kinase B (TrkB)/brain-derived neurotrophic factor system has been associated with psychiatric disorders, and animal models of defects in this system suggest that it might have a particular role in anxiety. Methods: DNA sequencing and cloning were used to identify a mutation in TrkB, and four different cell lines were used to assess functionality. Clinical samples were from a 22-year longitudinal cohort representative of the Quebec general population (n = 640 subjects), randomly selected when they were in kindergarten. Anxiety-related traits were measured with the Social Behaviour Questionnaire, the Diagnostic Assessment of Personality Pathology-Brief Questionnaire, and the Diagnostic Interview Schedule for DSM-IIIR. Results: An 11 base pair deletion in TrkB is significantly associated with increases in anxiety traits during childhood and the development of anxiety disorders in adulthood. We found that this deletion impaired transcription in some human cell lines. Conclusions: The identification of this deletion provides additional support for the role of TrkB in modulating anxiety-related traits in human.

引用

页码：604 / 607

页数：4

共 20 条

[1]

Deletion of TrkB in adult progenitors alters newborn neuron integration into hippocampal circuits and increases anxiety-like behavior [J].