China National Clinical Research Center for Neurological Diseases, Beijing Tiantan Hospital, Capital Medical University, Beijing, 100070, China.
College of Pharmaceutical Sciences, Capital Medical University, Beijing, 100070, China.
Acta Pharmacol Sin. 2019 May;40(5):571-582. doi: 10.1038/s41401-018-0185-5. Epub 2018 Dec 5.
Anxiety disorders arise from disruptions among the highly interconnected circuits that normally serve to process the streams of potentially threatening stimuli. The resulting imbalance among these circuits can cause a fundamental misinterpretation of neural sensory information as threatening and can lead to the inappropriate emotional and behavioral responses observed in anxiety disorders. There is considerable preclinical evidence that the GABAergic system, in general, and its α2- and/or α5-subunit-containing GABA(A) receptor subtypes, in particular, are involved in the pathophysiology of anxiety disorders. However, the clinical efficacy of GABA-A α2-selective agonists for the treatment of anxiety disorders has not been unequivocally demonstrated. In this review, we present several human pharmacological studies that have been performed with the aim of identifying the pharmacologically active doses/exposure levels of several GABA-A subtype-selective novel compounds with potential anxiolytic effects. The pharmacological selectivity of novel α2-subtype-selective GABA(A) receptor partial agonists has been demonstrated by their distinct effect profiles on the neurophysiological and neuropsychological measurements that reflect the functions of multiple CNS domains compared with those of benzodiazepines, which are nonselective, full GABA(A) agonists. Normalizing the undesired pharmacodynamic side effects against the desired on-target effects on the saccadic peak velocity is a useful approach for presenting the pharmacological features of GABA(A)-ergic modulators. Moreover, combining the anxiogenic symptom provocation paradigm with validated neurophysiological and neuropsychological biomarkers may provide further construct validity for the clinical effects of novel anxiolytic agents. In addition, the observed drug effects on serum prolactin levels support the use of serum prolactin levels as a complementary neuroendocrine biomarker to further validate the pharmacodynamic measurements used during the clinical pharmacological study of novel anxiolytic agents.
焦虑障碍源于高度相互关联的电路出现紊乱,这些电路通常用于处理潜在威胁性刺激的信息流。这些电路之间的不平衡会导致对神经感觉信息的基本误解,认为其具有威胁性,并可能导致焦虑障碍中观察到的不适当的情绪和行为反应。有大量临床前证据表明,GABA 能系统,一般来说,以及其包含α2-和/或α5-亚单位的 GABA(A) 受体亚型,特别是,参与了焦虑障碍的病理生理学。然而,GABA-Aα2-选择性激动剂治疗焦虑障碍的临床疗效尚未得到明确证实。在这篇综述中,我们介绍了几项已完成的人类药理学研究,旨在确定几种具有潜在抗焦虑作用的新型 GABA-A 亚型选择性化合物的药效学活性剂量/暴露水平。新型α2-亚型选择性 GABA(A) 受体部分激动剂的药理学选择性已通过其对神经生理和神经心理学测量的独特影响模式得到证明,这些测量反映了多个中枢神经系统区域的功能,与非选择性、全 GABA(A) 激动剂苯二氮䓬类药物不同。将对期望靶点的药效学作用与不期望的药效学副作用归一化,是呈现 GABA(A) 能调节剂药理学特征的一种有用方法。此外,将焦虑症状诱发范式与经过验证的神经生理学和神经心理学生物标志物相结合,可能为新型抗焦虑药物的临床疗效提供进一步的结构有效性。此外,观察到的药物对血清催乳素水平的影响支持将血清催乳素水平用作补充神经内分泌生物标志物,以进一步验证新型抗焦虑药物临床药理学研究中使用的药效学测量。