Lehner Małgorzata, Wisłowska-Stanek Aleksandra, Płaznik Adam
Zakład Neurochemii IPiN w Warszawie.
Psychiatr Pol. 2009 Nov-Dec;43(6):639-53.
Studies on the neurobiological background of anxiety indicate that the patogenesis of anxiety may be related to the process of an extinction of aversive memories. It has been suggested that disruption of selective attention for emotional stimuli may confer the risk for mental disorders, such as phobias and post-traumatic stress disorder, PTSD. Differences in the effects of local neuronal and hormonal activities of the HPA axis on emotional memory formation, might underlie individual differences in the emotional reactivity. Studies on molecular and cellular mechanisms responsible for individual fear extinction may serve as the basis of search for more effective forms of clinical treatment of anxiety. Behavioural therapy of phobias and PTSD can be facilitated by D-cycloserine (the agonist at the glycine site of the NMDA receptor), ligands stimulating endogenous cannabinoid system and by gluocorticosteroids. Although all these substances stimulate different central mechanisms, they appear to act synergistically, to improve the behavioural therapy.
关于焦虑症神经生物学背景的研究表明，焦虑症的发病机制可能与厌恶记忆的消退过程有关。有人提出，对情绪刺激的选择性注意力中断可能会使人患上精神障碍，如恐惧症和创伤后应激障碍（PTSD）。下丘脑 - 垂体 - 肾上腺（HPA）轴的局部神经元和激素活动对情绪记忆形成的影响存在差异，这可能是情绪反应个体差异的基础。对个体恐惧消退的分子和细胞机制的研究可能为寻找更有效的焦虑症临床治疗形式提供依据。D - 环丝氨酸（NMDA受体甘氨酸位点的激动剂）、刺激内源性大麻素系统的配体以及糖皮质激素可促进恐惧症和创伤后应激障碍的行为治疗。尽管所有这些物质刺激不同的中枢机制，但它们似乎具有协同作用，以改善行为治疗效果。
