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CCK‐4‐Induced Calcium Mobilization in T Cells Is Enhanced in Panic Disorder
Author(s) -
Akiyoshi Jotaro,
Moriyama Tamie,
Isogawa Koichi,
Miyamoto Masafumi,
Sasaki Ichiro,
Kuga Kiyomi,
Yamamoto Hisao,
Yamada Kenji,
Fujii Isao
Publication year - 1996
Publication title -
journal of neurochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.75
H-Index - 229
eISSN - 1471-4159
pISSN - 0022-3042
DOI - 10.1046/j.1471-4159.1996.66041610.x
Subject(s) - cholecystokinin , endocrinology , medicine , calcium , cholecystokinin receptor , calcium in biology , protein kinase c , cholecystokinin b receptor , chemistry , receptor , biology , signal transduction , biochemistry
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 a 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.