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[从惊恐发作的诱发因素到惊恐障碍的神经生物学]

[From inducers of panic attack to neurobiology of panic disorder].

作者信息

Bourin M

机构信息

Groupe de Recherche Neurobiologie de l'anxiété, Université de Nantes.

出版信息

Encephale. 1996 Dec;22 Spec No 5:35-41.

PMID:9138945
Abstract

Various provocative agents, including sodium lactate, carbon dioxide (CO2), caffeine, yohimbine and cholecystokinin (CCK), have been utilized as panicogenics in studies on healthy volunteers as well as in panic disorder patients. Most provocative agents are lacking in specificity, limiting their use in identifying neurotransmitter systems involved in panic attacks. CCK appears to offer several advantages over other challenge strategies since it is a putative neurotransmitter in the CNS, with its own neuronal pathways and receptors, and reliably provokes panic attacks in a dose-dependent manner. It is important to clarify the relationships between CCK and other neurotransmitter systems in order to further understand the neurobiology of panic disorder. The possible roles of some of these neurotransmitters in panic disorder are discussed in this review.

摘要

包括乳酸钠、二氧化碳(CO₂)、咖啡因、育亨宾和胆囊收缩素(CCK)在内的多种激发剂,已被用作在健康志愿者以及惊恐障碍患者研究中的致惊恐剂。大多数激发剂缺乏特异性,限制了它们在识别惊恐发作所涉及的神经递质系统方面的应用。与其他激发策略相比,CCK似乎具有几个优势,因为它是中枢神经系统中的一种假定神经递质,有其自身的神经元通路和受体,并且能以剂量依赖的方式可靠地引发惊恐发作。为了进一步理解惊恐障碍的神经生物学,阐明CCK与其他神经递质系统之间的关系很重要。本综述讨论了其中一些神经递质在惊恐障碍中的可能作用。

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