一项新的研究结果显示了人脑在一项恐惧条件反射实验期间的焦虑状况，并揭示了为何有些人更容易或者更不容易罹患焦虑症。
这项发表在《神经元》Neuron 月刊2月号上的研究结果揭示，神经机制可能与抵抗病理性恐惧和焦虑的能力相关。这项发现或许有助于改进慢性焦虑症的治疗方法，也有助于指导危险个体找到避免罹患焦虑症的方法。
此前的一些研究结果显示扁桃核这一脑结构与获得和表达条件性恐惧有关。条件性恐惧指某种刺激(条件刺激)变得与某个令人厌恶的物体或者事件(无条件刺激)相关的状况。研究结果显示，不管在动物还是人体内，另一个脑区域——腹内侧前额叶皮质都有助于在恐惧消退训练后阻止条件性恐惧。恐惧消退训练指不断发出条件刺激，却不呈现无条件刺激。
这项研究报告的高级作者、美国加利福尼亚大学伯克利分校的索尼娅·J·毕晓普博士解释说：“我们对为何有些人能比其他人更容易克服在生活中经历的个别恐惧和非特定焦虑有兴趣。换句话说，要确定脑功能上的哪些区别可能导致某些人更容易罹患慢性恐惧和焦虑症。”
毕晓普及其同事开展了一项神经成像项目来研究人的恐惧条件反射。这些研究对象被归为具有不同程度“个性焦虑”的一类人，他们具有在一系列日常环境中发生焦虑的倾向。研究人员发现，个性焦虑程度高的研究对象的扁桃核更可能对条件刺激恐惧暗示作出强烈反应，并显示能更快地获取这些暗示的“习得性恐惧”。（生物谷Bioon.com）
生物谷推荐原文出处：
Neuron doi:10.1016/j.neuron.2010.12.034
Fear-Conditioning Mechanisms Associated with Trait Vulnerability to Anxiety in Humans
Iole Indovina, Trevor W. Robbins, Anwar O. Nú?ez-Elizalde, Barnaby D. Dunn, Sonia J. Bishop
Summary
Investigations of fear conditioning in rodents and humans have illuminated the neural mechanisms underlying cued and contextual fear. A critical question is how personality dimensions such as trait anxiety act through these mechanisms to confer vulnerability to anxiety disorders, and whether humans' ability to overcome acquired fears depends on regulatory skills not characterized in animal models. In a neuroimaging study of fear conditioning in humans, we found evidence for two independent dimensions of neurocognitive function associated with trait vulnerability to anxiety. The first entailed increased amygdala responsivity to phasic fear cues. The second involved impoverished ventral prefrontal cortical (vPFC) recruitment to downregulate both cued and contextual fear prior to omission (extinction) of the aversive unconditioned stimulus. These two dimensions may contribute to symptomatology differences across anxiety disorders; the amygdala mechanism affecting the development of phobic fear and the frontal mechanism influencing the maintenance of both specific fears and generalized anxiety.
