Serotonin-induced platelet intracellular calcium mobilization in various psychiatric disorders: is it specific to bipolar disorder?

被引:40
作者
Suzuki, K [1 ]
Kusumi, I [1 ]
Sasaki, Y [1 ]
Koyama, T [1 ]
机构
[1] Hokkaido Univ, Sch Med, Dept Psychiat, Sapporo, Hokkaido 0608638, Japan
关键词
bipolar disorder; serotonin; serotonin 5-HT2A receptor; calcium; platelet; signal transduction;
D O I
10.1016/S0165-0327(00)00221-4
中图分类号
R74 [神经病学与精神病学];
学科分类号
摘要
Background: Serotonin (5-HT)-stimulated platelet intracellular calcium (Ca) mobilization has been reported to be enhanced in unmedicated depressive patients compared to those of normal healthy subjects, which suggests increased 5-HT2A receptor function in these patients. It has not been ascertained whether this enhanced response is specific to some type of affective disorders among various mental disorders. Methods: We examined 5-HT-induced platelet intracellular Ca response in 152 unmedicated outpatients with various psychiatric disorders including bipolar disorder (BD), major depressive disorder with melancholia (DM), major depressive disorder without melancholia (DN), schizophrenia (SCH), panic disorder (PD), obsessive-compulsive disorder (OCD), social phobia (SP) and bulimia nervosa (BN), and 30 normal controls. Results: We observed no significant differences in basal intracellular Ca concentration among all patient subgroups and normal controls. While the 5-HT-induced Ca response was significantly and specifically higher in patients with ED than in normal controls, no significant differences were found in the Ca response to 5-HT between patients with DM, DN, SCH, PD, OCD, SP and BN, and normal controls. Limitations: The sample sizes of each group are still small. Therefore, they have to be enlarged in the continuation of the study so as to increase the power of the statistical tests. Conclusion: These results indicate the possibility that enhanced signal transduction, mediated by the 5-HT2A receptor, may be specific to bipolar disorder. (C) 2001 Elsevier Science B;V. All rights reserved.
引用
收藏
页码:291 / 296
页数:6
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