Department of Psychiatry and Psychotherapy, University of Marburg, Marburg, Germany; Center for Mind, Brain and Behavior (CMBB), University of Marburg and Justus Liebig University Giessen, Germany.
Institute of Psychology, University of Greifswald, Greifswald, Germany.
Eur Neuropsychopharmacol. 2019 Oct;29(10):1138-1151. doi: 10.1016/j.euroneuro.2019.07.133. Epub 2019 Aug 20.
The gene coding for glycine receptor β subunits (GLRB) has been found to be related to panic disorder and agoraphobia (PD/AG) and to be associated with altered insular BOLD activation during fear conditioning, as an intermediate phenotype of defensive system reactivity in healthy subjects. In a multicenter clinical trial on PD/AG patients we investigated in three sub-samples whether GLRB allelic variation (A/G; A-allele identified as «risk») in the single nucleotide polymorphism rs7688285 was associated with autonomic (behavioral avoidance test BAT; n = 267 patients) and neural (differential fear conditioning; n = 49 patients, n = 38 controls) measures, and furthermore with responding towards exposure-based cognitive behavioral therapy (CBT, n = 184 patients). An interaction of genotype with current PD/AG diagnosis (PD/AG vs. controls; fMRI data only) and their modification after CBT was tested as well. Exploratory fMRI results prior to CBT, revealed A-allele carriers irrespective of diagnostic status to show overall higher BOLD activation in the hippocampus, motor cortex (MC) and insula. Differential activation in the MC, anterior cingulate cortex (ACC) and insula was found in the interaction genotype X diagnosis. Differential activation in ACC and hippocampus was present in differential fear learning. ACC activation was modified after treatment, while no overall rs7688285 dependent effect on clinical outcomes was found. On the behavioral level, A-allele carriers showed pronounced fear reactivity prior to CBT which partially normalized afterwards. In sum, rs7688285 variation interacts in a complex manner with PD/AG on a functional systems level and might be involved in the development of PD/AG but not in their treatment.
甘氨酸受体β亚基(GLRB)基因编码已被发现与惊恐障碍和广场恐怖症(PD/AG)有关,并与健康受试者防御系统反应的中间表型有关,即在恐惧条件反射期间岛叶 BOLD 激活改变。在一项针对 PD/AG 患者的多中心临床试验中,我们在三个亚样本中研究了 GLRB 单核苷酸多态性 rs7688285 的等位基因变异(A/G;A 等位基因被鉴定为“风险”)是否与自主神经(行为回避测试 BAT;n = 267 名患者)和神经(差异恐惧条件反射;n = 49 名患者,n = 38 名对照)测量有关,并且与基于暴露的认知行为治疗(CBT,n = 184 名患者)的反应有关。还测试了基因型与当前 PD/AG 诊断(PD/AG 与对照;仅 fMRI 数据)的相互作用及其在 CBT 后的修饰,以及 CBT 前的探索性 fMRI 结果,无论诊断状态如何,A 等位基因携带者在海马体、运动皮层(MC)和岛叶中总体显示出更高的 BOLD 激活。在基因型 X 诊断的相互作用中发现了 MC、前扣带皮层(ACC)和岛叶的差异激活。在差异恐惧学习中存在 ACC 和海马体的差异激活。ACC 激活在治疗后发生改变,而在 rs7688285 依赖性临床结果方面未发现总体影响。在行为水平上,A 等位基因携带者在 CBT 前表现出明显的恐惧反应,之后部分恢复正常。总之,rs7688285 变异以复杂的方式与 PD/AG 在功能系统水平上相互作用,可能与 PD/AG 的发生有关,但与治疗无关。