Max Planck Institute of Experimental Medicine, Department of Molecular Neurobiology, Göttingen, Germany.
Mol Med. 2013 Jul 24;19(1):135-48. doi: 10.2119/molmed.2013.00033.
Anxiety disorders and substance abuse, including benzodiazepine use disorder, frequently occur together. Unfortunately, treatment of anxiety disorders still includes benzodiazepines, and patients with an existing comorbid benzodiazepine use disorder or a genetic susceptibility for benzodiazepine use disorder may be at risk of adverse treatment outcomes. The identification of genetic predictors for anxiety disorders, and especially for benzodiazepine use disorder, could aid the selection of the best treatment option and improve clinical outcomes. The brain-specific angiogenesis inhibitor I-associated protein 3 (Baiap3) is a member of the mammalian uncoordinated 13 (Munc13) protein family of synaptic regulators of neurotransmitter exocytosis, with a striking expression pattern in amygdalae, hypothalamus and periaqueductal gray. Deletion of Baiap3 in mice leads to enhanced seizure propensity and increased anxiety, with the latter being more pronounced in female than in male animals. We hypothesized that genetic variation in human BAIAP3 may also be associated with anxiety. By using a phenotype-based genetic association study, we identified two human BAIAP3 single-nucleotide polymorphism risk genotypes (AA for rs2235632, TT for rs1132358) that show a significant association with anxiety in women and, surprisingly, with benzodiazepine abuse in men. Returning to mice, we found that male, but not female, Baiap3 knockout (KO) mice develop tolerance to diazepam more quickly than control animals. Analysis of cultured Baiap3 KO hypothalamus slices revealed an increase in basal network activity and an altered response to diazepam withdrawal. Thus, Baiap3/BAIAP3 is gender specifically associated with anxiety and benzodiazepine use disorder, and the analysis of Baiap3/BAIAP3-related functions may help elucidate mechanisms underlying the development of both disorders.
焦虑障碍和物质滥用,包括苯二氮䓬类药物使用障碍,经常同时发生。不幸的是,焦虑障碍的治疗仍包括苯二氮䓬类药物,而同时存在共病性苯二氮䓬类药物使用障碍或苯二氮䓬类药物使用障碍遗传易感性的患者可能存在不良治疗结局的风险。焦虑障碍,特别是苯二氮䓬类药物使用障碍的遗传预测因子的鉴定,可以帮助选择最佳治疗方案并改善临床结局。脑特异性血管生成抑制剂 I 相关蛋白 3(Baiap3)是哺乳动物协调蛋白 13(Munc13)家族的成员,是神经递质释放的突触调节剂,在杏仁核、下丘脑和导水管周围灰质中具有显著的表达模式。在小鼠中删除 Baiap3 会导致癫痫发作倾向增强和焦虑增加,后者在雌性动物中比在雄性动物中更为明显。我们假设人类 BAIAP3 的遗传变异也可能与焦虑有关。通过使用基于表型的遗传关联研究,我们确定了两个与焦虑相关的人类 BAIAP3 单核苷酸多态性风险基因型(rs2235632 的 AA,rs1132358 的 TT),这些基因型在女性中与焦虑显著相关,在男性中与苯二氮䓬滥用显著相关。回到小鼠,我们发现雄性,但不是雌性,Baiap3 敲除(KO)小鼠比对照动物更快地对安定产生耐受性。对培养的 Baiap3 KO 下丘脑切片的分析显示,基础网络活动增加,对安定戒断的反应改变。因此,Baiap3/BAIAP3 性别特异性地与焦虑和苯二氮䓬类药物使用障碍相关,对 Baiap3/BAIAP3 相关功能的分析可能有助于阐明这两种疾病发展的机制。