胆囊收缩素与惊恐障碍：历史反思与未解问题探讨。
Cholecystokinin and Panic Disorder: Reflections on the History and Some Unsolved Questions.
机构信息
Department of Clinical Biochemistry, Rigshospitalet, University of Copenhagen, DK-2100 Copenhagen, Denmark.
出版信息
Molecules. 2021 Sep 17;26(18):5657. doi: 10.3390/molecules26185657.
The classic gut hormone cholecystokinin (CCK) and its CCK-receptor are expressed in almost all regions of the brain. This widespread expression makes CCK by far the most abundant peptidergic transmitter system in the brain. This CNS-ubiquity has, however, complicated the delineation of the roles of CCK peptides in normal brain functions and neuropsychiatric diseases. Nevertheless, the common panic disorder disease is apparently associated with CCK in the brain. Thus, the C-terminal tetrapeptide fragment of CCK (CCK-4) induces, by intravenous administration in a dose-related manner, panic attacks that are similar to the endogenous attacks in panic disorder patients. This review describes the history behind the discovery of the panicogenic effect of CCK-4. Subsequently, the review discusses three unsettled questions about the involvement of cerebral CCK in the pathogenesis of anxiety and panic disorder, including therapeutic attempts with CCK-receptor antagonists.
经典的肠道激素胆囊收缩素 (CCK) 及其 CCK 受体几乎存在于大脑的所有区域。这种广泛的表达使 CCK 成为迄今为止大脑中最丰富的肽能递质系统。然而，这种中枢神经系统的普遍性使得 CCK 肽在正常大脑功能和神经精神疾病中的作用难以确定。尽管如此，常见的恐慌症疾病显然与大脑中的 CCK 有关。因此，CCK（CCK-4）的 C 端四肽片段以剂量相关的方式通过静脉内给药诱导类似于恐慌症患者内源性发作的恐慌发作。本综述描述了发现 CCK-4 致惊恐作用背后的历史。随后，该综述讨论了关于大脑 CCK 参与焦虑和恐慌症发病机制的三个悬而未决的问题，包括使用 CCK 受体拮抗剂进行的治疗尝试。
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