Neuropharmacology of buspirone.
Neuropharmacology of buspirone.
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丁螺环酮的神经药理学。
DOI：
10.1159/000284133
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发表时间：
1984
期刊：
影响因子：
3.6
通讯作者：
C. P. Vandermaelen
中科院分区：
文献类型：
--
作者：
L. Riblet;A. S. Eison;M. Eison;Duncan P. Taylor;D. Temple;C. P. Vandermaelen
丁螺环酮是一种临床有效的抗焦虑药，具有独特的结构和药理学，使其与苯二氮卓类药物不同。它被称为抗焦虑选择性，因为它缺乏抗惊厥，镇静或肌肉松弛的特性。临床前证据表明，它缺乏滥用或身体依赖的可能性，与中枢神经系统抑制剂（如酒精）的相互作用极小。丁螺环酮不是通过传统的苯二氮卓类机制发挥作用，而是影响大脑神经化学回路的各个方面。例如，它对黑质纹状体和中脑边缘多巴胺系统、中缝背核多巴胺能系统和蓝斑去甲肾上腺素能系统产生强有力的影响。虽然没有直接的受体相互作用，胆碱能介导的行为和参与GABA能神经传递的增强也已被证明。
Buspirone is a clinically effective anxiolytic with a unique structure and pharmacology which distinguishes it from the benzodiazepines. It has been termed anxioselective because it lacks anticonvulsant, sedative, or muscle-relaxant properties. Preclinical evidence suggests it lacks potential for abuse or physical dependence and interacts minimally with CNS depressants such as alcohol. Rather than working through traditional benzodiazepine mechanisms, buspirone affects diverse aspects of the brain's neurochemical circuitry. For example, it exerts potent influences on the nigrostriatal and mesolimbic dopamine systems, the dorsal raphe serotonergic system, and the locus coeruleus noradrenergic system. Although without direct receptor interaction, potentiation of cholinergically mediated behavior and involvement with GABAergic neurotransmission have also been demonstrated.