CCK-4-induced calcium mobilization in T cells is enhanced in panic disorder

• Published in: Journal of neurochemistry Vol. 66; no. 4; p. 1610
• Main Authors: Akiyoshi, J, Moriyama, T, Isogawa, K, Miyamoto, M, Sasaki, I, Kuga, K, Yamamoto, H, Yamada, K, Fujii, I
• Format: Journal Article
• Language: English
• Published: England 01.04.1996
• Subjects: Adult; Alprazolam - pharmacology; Biomarkers; Calcium - metabolism; Dose-Response Relationship, Drug; Female; Humans; Male; Middle Aged; Nootropic Agents - pharmacology; Panic Disorder - immunology; Panic Disorder - metabolism; Pentagastrin - pharmacology; Receptors, Cholecystokinin - drug effects; Receptors, Cholecystokinin - metabolism; Sincalide - analogs & derivatives; Sincalide - pharmacology; T-Lymphocytes - drug effects; T-Lymphocytes - metabolism; T-Lymphocytes - ultrastructure; Tetragastrin - agonists; Tetragastrin - antagonists & inhibitors; Tetragastrin - pharmacology
• ISSN: 0022-3042
• DOI: 10.1046/j.1471-4159.1996.66041610.x

We investigated the effects of brain cholecystokinin (CCK) receptors on the intracellular calcium concentration and protein kinase C in human T cells. CCK-4 produced a transient increase in calcium in the absence of extracellular calcium. CCK-B agonists stimulated calcium mobilization in a dose-dependent manner in T cells. CCK-B antagonists suppressed CCK-4-induced calcium mobilization more potently than CCK-A antagonist. The recovery of desensitization of the CCK-4-induced response was delayed by phosphoserine/phosphothreonine phosphatase inhibitor, calyculin A. The responsiveness to CCK-4 was also reduced by phorbol 12,13-dibutyrate (PDBu), and this effect of PDBu was abolished completely by preincubation with staurosporine. CCK-4-induced calcium mobilization was too small to attribute the desensitization to the protein kinase C transduction pathway. T cells from patients with untreated panic disorder exhibited significantly higher cholecystokinin-4-induced calcium mobilization than those from healthy controls or patients with treated panic disorder. These results suggest that cholecystokinin-B receptor function in T cells of patients with panic disorder is enhanced. Cholecystokinin-4-induced calcium mobilization in T cells may be state dependent and useful as a biological marker of panic disorder.