There have been several researches on the role of personality in the pathophysiology of bipolar disorder. Recently, a polymorphism of XBP1, a pivotal gene in the endoplasmic reticulum (ER) stress response, was shown to contribute to the genetic risk factor for bipolar disorder. Therefore, in this study, we examined the relationship between the XBP1 gene polymorphism and the personality traits assessed by two self-rating scales, a shortened version of Temperament and Character Inventory (TCI) and NEO-Five Factor Inventory (NEO-FFI) in healthy subjects. The present results suggested that the XBP1 gene polymorphism was associated with the NEO-FFI score of neuroticism in female subjects. However, no significant differences in the other personality scale scores of both assessments were observed among normal subjects with -116C/C, C/G and G/G genotypes. Further investigations are necessary to examine the relationship in patients with bipolar disorder, or use full version of various self-rating personality assessments
Abstract:Disturbed intracellular calcium (Ca 2+ ) homeostasis has been implicated in bipolar disorder, which mechanisms may be involved in the dysregulation of protein kinase C (PKC) and calmodulin systems. In this study, we investigated a transient intracellular Ca 2+ increase induced by thapsigargin, a inhibitor of sarco/endoplasmic reticulum Ca 2+ -ATPase pump (SERCA), and a capacitative Ca 2+ entry followed by addition of extracellular Ca 2+ , in the presence or absence of PKC/calmodulin modulators in the platelets of healthy subjects in order to elucidate the role of SERCA in Ca 2+ homeostasis and to assess how both PKC and calmodulin systems regulate the two Ca 2+ responses. Moreover, we also examined the thapsigargin-elicited transient Ca 2+ increase and capacitative Ca 2+ entry in patients with mood disorders. PKC and calmodulin systems have opposite regulatory effects on the transient Ca 2+ increase and capacitative Ca 2+ entry in the platelets of normal subjects. The inhibitory effect of PKC activation on capacitative Ca 2+ entry is significantly increased and the stimulatory effect of PKC inhibition is significantly decreased in bipolar disorder compared to major depressive disorder and normal controls. These results suggest the possibility that increased PKC activity may activate the inhibitory effect of capacitative Ca 2+ entry in bipolar disorder. However, this is a preliminary study using a small sample, thus further studies are needed to examine the PKC and calmodulin modulators on the capacitative Ca 2+ entry in a larger sample.
We have reported that the platelet intracellular calcium (Ca) mobilization after stimulation by serotonin (5-HT) is specifically enhanced in bipolar disorder among various psychiatric disorders, compared with that in normal control. To explore the mechanisms of enhanced Ca response to 5-HT in the platelets, we first examined the relation between the 5HT-elicited Ca mobilization and 5-HT 2A receptor density using the platelets from 13 normal subjects. From this study, we found no significant correlation between two measures. Then, we investigated the effects of staurosporine, a protein kinase C (PKC) inhibitor, on Ca response to 5-HT in platelets from patients with major depressive disorder (unipolar), bipolar disorder, and normal controls. While 5-HT-induced Ca mobilization, in the presence of 100 nM staurosporine, was significantly attenuated in normal controls and patients with major depressive disorder, the inhibitory effect of staurosporine was not observed in bipolar disorder. These results suggest that the failure in inhibiting the platelet intracellular Ca response to 5-HT in bipolar disorder may be related to increased activity of PKC rather than increased 5-HT 2A receptor number. Moreover, the trend of the Ca response towards staurosporine may become a specific biological marker for unipolar-bipolar dichotomy.
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