Eison A S, Temple D L
Am J Med. 1986 Mar 31;80(3B):1-9. doi: 10.1016/0002-9343(86)90325-6.
Buspirone is a novel anxiolytic agent unrelated to the benzodiazepines in structure or pharmacologic properties. Extensive clinical studies have shown buspirone to be effective in the treatment of anxiety, with efficacy comparable to diazepam or clorazepate. Buspirone exhibits a unique pharmacologic profile in that it alleviates anxiety without causing sedation or functional impairment and does not promote abuse or physical dependence. Furthermore, preclinical studies have shown that buspirone does not possess anticonvulsant or muscle relaxant properties and does not interact significantly with central nervous system depressants. Biochemical and electrophysiologic studies indicate that buspirone alters monoaminergic and GABAergic systems in a manner different from that of the benzodiazepines. The uniform depressant action of the benzodiazepines upon serotonergic, noradrenergic, and dopaminergic cell firing may result from their facilitatory effect on gamma-aminobutyric acid and its known inhibitory influence in these monoaminergic areas. Unlike the benzodiazepines, buspirone exerts a differential influence upon monoaminergic neuronal activity, suppressing serotonergic activity while enhancing dopaminergic and noradrenergic cell firing. The mechanism of action of buspirone challenges the notion that only one neurotransmitter mediates anxiety. The interaction with multiple neurotransmitters at multiple brain sites suggests that buspirone may alter diverse activities within a "neural matrix of anxiety." In contrast to the benzodiazepines, buspirone orchestrates activity within this neural matrix to achieve effective treatment of anxiety while preserving arousal and attentional processes.
丁螺环酮是一种新型抗焦虑药，其结构和药理特性与苯二氮䓬类药物无关。广泛的临床研究表明，丁螺环酮在治疗焦虑症方面有效，疗效与地西泮或氯氮䓬相当。丁螺环酮具有独特的药理特性，即它能缓解焦虑而不引起镇静或功能损害，也不会导致药物滥用或身体依赖。此外，临床前研究表明，丁螺环酮不具有抗惊厥或肌肉松弛特性，且与中枢神经系统抑制剂无明显相互作用。生化和电生理研究表明，丁螺环酮改变单胺能和γ-氨基丁酸能系统的方式与苯二氮䓬类药物不同。苯二氮䓬类药物对血清素能、去甲肾上腺素能和多巴胺能细胞放电的一致抑制作用可能源于它们对γ-氨基丁酸的促进作用及其在这些单胺能区域已知的抑制影响。与苯二氮䓬类药物不同，丁螺环酮对单胺能神经元活动有不同的影响，抑制血清素能活动，同时增强多巴胺能和去甲肾上腺素能细胞放电。丁螺环酮 的作用机制挑战了只有一种神经递质介导焦虑的观念。在多个脑区与多种神经递质的相互作用表明，丁螺环酮可能改变“焦虑神经基质”内的多种活动。与苯二氮䓬类药物不同，丁螺环酮在这个神经基质内协调活动，以实现对焦虑症的有效治疗，同时保持觉醒和注意力过程。
