Serotonin-induced platelet calcium mobilization is enhanced in mania
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Cited by (65)
From intracellular signaling pathways to neural circuit dysfunction in bipolar disorder
2020, Neurobiology of Bipolar Disorder: Road to Novel TherapeuticsIncreased platelet intracellular calcium ion concentration is specific to bipolar disorder
2014, Journal of Affective DisordersCitation Excerpt :Since the first demonstration of increased intracellular calcium signaling in peripheral cells of patients with bipolar disorder (Dubovsky et al., 1989) in the absence of changes in cereberospinal fluid and serum calcium ion (Ca2+) concentration (Yatham et al., 1997) a number of studies (for exceptions see Bothwell et al. (1994)) have confirmed increased resting ([Ca2+]B) free intracellular calcium ion concentration ([Ca2+]i) in patients with bipolar disorder compared with controls in blood platelets, lymphocytes, B-lymphoblast cell lines (BLCLs), and neuroblastoma cells, as well as an elevation of intracellular calcium ion concentration stimulated by agonists ([Ca2+]s), including thrombin, platelet activating factor (PAF), serotonin, dopamine, thapsigargin and various mitogens (Dubovsky et al., 1992b; Hough et al., 1999; Perova et al., 2008; Quiroz et al., 2008; Schreiber et al., 1991; So et al., 2007). Most studies that demonstrate increased resting and/or agonist stimulated [Ca2+]i in bipolar disorder have reported similar elevations in mania and bipolar depression (Dubovsky et al., 1989, 1991a, 1991b, 1992c; Hahn et al., 2005; Hough et al., 1999; Kusumi et al., 1994b; Okamoto et al., 1995; Perova et al., 2008). When bipolar I and bipolar II disorders have been compared, the results have been similar in some (Hough et al., 1999) if not all (Emamghoreishi et al., 1997) studies.
Effects of calmodulin and protein kinase C modulators on transient Ca<sup>2+</sup> increase and capacitative Ca<sup>2+</sup> entry in human platelets: Relevant to pathophysiology of bipolar disorder
2007, Progress in Neuro-Psychopharmacology and Biological PsychiatryCitation Excerpt :We have reported that serotonin (5-HT)- or thrombin-induced intraplatelet Ca2+ mobilization is enhanced in unmedicated patients with bipolar disorder (Kusumi et al., 1992, 1994; Suzuki et al., 2001). Other researchers have indicated similar findings (Dubovsky et al., 1991; Okamoto et al., 1995). Moreover, the 5-HT-stimulated Ca2+ response is significantly attenuated in the presence of staurosporine, a protein kinase C (PKC) inhibitor, in normal controls and major depressive disorder, whereas the inhibitory effect of staurosporine is not observed in bipolar disorder (Suzuki et al., 2003).
Animal models of bipolar disorder
2007, Neuroscience and Biobehavioral ReviewsDistinctions between bipolar and unipolar depression
2005, Clinical Psychology Review