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The role of the ‘central’ cholecystokinin-B receptor in panic disorder

Published online by Cambridge University Press:  18 September 2015

H.J.G.M. Van Megen*
Affiliation:
Rudolf Magnus Institute of Neurosciences
H.G.M. Westenberg
Affiliation:
Rudolf Magnus Institute of Neurosciences
J.A. Den Boer
Affiliation:
Afdeling Biologische Psychiatrie, Academisch ziekenhuis Groningen, 9700 RB Groningen
*
Rudolf Magnus Institute of Neurosciences, Dept. of Psychiatry, University Hospital Utrecht, P.O. Box 85500, 3508 GA Utrecht

Summary

Research investigating the neurobiological underpinnings of anxiety disorder have mainly been focused on dysfunction of the GABA, noradrenergic and serotonergic (5-HT) neuronal systems. Just recently, in both animal and human studies, evidence has been found for a possible role of the cholecystokinin (CCK) neuronal system in the pathogenesis of anxiety disorder.

Behaviorally, animal studies revealed anxiogenic-like properties for the ‘central’ CCKB receptor agonists, while CCKB receptor antagonists displayed intrinsic anxiolytic properties. Similarly, in man, CCKB receptor agonists, like pentagastrin and CCK4, were found to be able to elicited panic attacks in both panic disorder (PD) patients and healthy volunteers. These effects appear due to stimulation of the CCKB receptor. In addition, clinically effective panicolytic agents reduce the sensitivity to CCK4 in PD patients. Taken together, these findings may suggest a role for CCK in the neurobiology of PD. On the other hand, there is circumstantial evidence for involvement of several other neuronal systems, such as the serotonergic, noradrenergic and GABA-ergic system, in the regulation of anxiety. Interestingly, evidence has been found for an interaction between CCK and 5-HT and that this interaction plays a role in the mediation of anxiety.

This presentation will critically discuss the evidence for the role of the CCKB receptor in anxiety and in addition, will focus on the putative evidence that the role of CCK in anxiety is mediated by its interaction with the serotonergic neuronal system.

Type
Research Article
Copyright
Copyright © Scandinavian College of Neuropsychopharmacology 1996

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References

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