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Rigshospitalet - a part of Copenhagen University Hospital
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Cholecystokinin and panic disorder: reflections on the history and some unsolved questions

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  1. Evaluation of a 68Ga-Labeled DOTA-Tetrazine as a PET Alternative to 111In-SPECT Pretargeted Imaging

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  1. Entero-pancreatic hormone secretion, gastric emptying, and glucose absorption after frequently sampled meal tests

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  2. Liraglutide decreases postprandial fibroblast growth factor 19 and glucagon-like peptide 2, and increases postprandial cholecystokinin in individuals with obesity

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  3. Acute ketosis inhibits appetite and decreases plasma concentrations of acyl ghrelin in healthy young men

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  4. Expression of cholecystokinin and its receptors in the intestinal tract of type 2 diabetes patients and healthy controls

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  5. Gastrin and the moderate hypergastrinemias

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The classic gut hormone cholecystokinin (CCK) and its CCK2-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 CCK2-receptor antagonists.

Original languageEnglish
Article number5657
JournalMolecules
Volume26
Issue number18
ISSN1420-3049
DOIs
Publication statusPublished - 17 Sep 2021

ID: 68616779