Amygdala-dependent fear conditioning in humans is modulated by the BDNFval66met polymorphism.
Amygdala-dependent fear conditioning in humans is modulated by the BDNFval66met polymorphism.
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DOI：
10.1037/a0018261
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发表时间：
2010-02
影响因子：
1.9
通讯作者：
Ohman, Arne
中科院分区：
文献类型：
--
作者：
Lonsdorf, Tina B.;Weike, Almut I.;Golkar, Armita;Schalling, Martin;Hamm, Alfons O.;Ohman, Arne
脑源性神经营养因子（BDNF）在神经可塑性以及海马和杏仁核依赖性学习的获得、巩固和保留中起着至关重要的作用。人类BDNF基因前结构域的A→G单核苷酸多态性（BDNFval66met）与细胞内转运异常和活性依赖性BDNF释放减少有关。我们在57名健康参与者中研究了BDNFval66met在厌恶差异恐惧条件反射和延迟消退范式中的作用。以男性面部图片作为刺激，恐惧学习通过恐惧增强惊吓（FPS）和皮肤电导反应（SCR）进行量化。有意识的BDNF基因携带者在杏仁核依赖的恐惧条件反射中表现出行为缺陷，这表明在最后一个习得区块中缺乏FPS反应。这一缺陷在第一次灭绝中得以维持。条件SCR歧视无基因型差异。这些数据为BDNF信号参与人类杏仁核依赖性学习提供了证据。我们认为BDNF met等位基因可能对情感病理的发展具有保护作用，这种病理是通过负面体验引起的突触可塑性降低来介导的。
The Brain derived neurotrophic factor (BDNF) is critically involved in neuroplasticity as well as the acquisition, consolidation, and retention of hippocampal- and amygdala-dependent learning. A common functional A→G single nucleotide polymorphism (BDNFval66met) in the pro-domain of the human BDNF gene is associated with abnormal intracellular trafficking and reduced activity-dependent BDNF release. We studied the effect of BDNFval66met in an aversive differential fear conditioning, and a delayed extinction paradigm in fifty-seven healthy participants. Pictures of male faces were used as stimuli and fear learning was quantified by fear potentiated startle (FPS) and skin conductance responses (SCR). Aware BDNF met-carriers show a behavioral deficit in amygdala-dependent fear conditioning as indicated by an absence of FPS responses in the last acquisition block. This deficit was maintained in the first block of extinction. No genotype differences were found in conditioned SCR discrimination. These data provide evidence for the involvement of BDNF signaling in human amygdala-dependent learning. We suggest that the BDNF met-allele may have a protective effect for the development of affective pathologies that is mediated via reduced synaptic plasticity induced by negative experience.
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