Steven L Dubovsky1, Elsa Daurignac2, Kenneth E Leonard3. 1. Department of Psychiatry, State University of New York at Buffalo, Buffalo, NY 14215, USA; Departments of Psychiatry and Medicine, University of Colorado, Denver, CO, USA. Electronic address: dubovsky@buffalo.edu. 2. Department of Psychiatry, State University of New York at Buffalo, Buffalo, NY 14215, USA. 3. Department of Psychiatry, State University of New York at Buffalo, Buffalo, NY 14215, USA; Research Institute on Addictions, University at Buffalo, Buffalo, NY, USA.
Abstract
BACKGROUND: Increased baseline ([Ca(2+)]B) and agonist-stimulated ([Ca(2+)]s) free intracellular calcium ion concentrations ([Ca(2+)]i) are well-replicated findings in bipolar disorder, but whether this finding is specific to that condition and if so, whether it is a marker of the mood disorder or a feature seen in other disorders such as psychosis has remained unclear. METHODS: Platelet [Ca(2+)]i was assessed in 15 inpatients with psychotic and nonpsychotic mania, 17 schizophrenia inpatients, and 17 matched controls. RESULTS: Platelet [Ca(2+)]B and [Ca(2+)]s were significantly higher than controls in bipolar disorder but not schizophrenia. Variability of [Ca(2+)]B was significantly increased in bipolar disorder regardless of the presence of psychosis, but not in schizophrenia. LIMITATIONS: Use of antipsychotic drugs by the majority of both patient groups may have obscured elevated [Ca(2+)]i in schizophrenia, or may have masked a difference between psychotic and nonpsychotic bipolar disorder. Measurement of [Ca(2+)]i is too labor intensive to become a routine test for diagnosis or prediction of treatment response. CONCLUSIONS: Elevated intracellular Ca(2+) signaling may be a marker of primary cellular hyperactivity that could contribute to comorbid conditions such as hypertension and neuronal apoptosis. Since lithium and carbamazepine attenuate increased [Ca(2+)]i, further research may demonstrate a correlation between normalization of [Ca(2+)]i and response to one of these medications, and further research may clarify whether a subgroup of patients may respond well to calcium channel antagonists.
BACKGROUND: Increased baseline ([Ca(2+)]B) and agonist-stimulated ([Ca(2+)]s) free intracellular calcium ion concentrations ([Ca(2+)]i) are well-replicated findings in bipolar disorder, but whether this finding is specific to that condition and if so, whether it is a marker of the mood disorder or a feature seen in other disorders such as psychosis has remained unclear. METHODS: Platelet [Ca(2+)]i was assessed in 15 inpatients with psychotic and nonpsychotic mania, 17 schizophrenia inpatients, and 17 matched controls. RESULTS: Platelet [Ca(2+)]B and [Ca(2+)]s were significantly higher than controls in bipolar disorder but not schizophrenia. Variability of [Ca(2+)]B was significantly increased in bipolar disorder regardless of the presence of psychosis, but not in schizophrenia. LIMITATIONS: Use of antipsychotic drugs by the majority of both patient groups may have obscured elevated [Ca(2+)]i in schizophrenia, or may have masked a difference between psychotic and nonpsychotic bipolar disorder. Measurement of [Ca(2+)]i is too labor intensive to become a routine test for diagnosis or prediction of treatment response. CONCLUSIONS: Elevated intracellular Ca(2+) signaling may be a marker of primary cellular hyperactivity that could contribute to comorbid conditions such as hypertension and neuronal apoptosis. Since lithium and carbamazepine attenuate increased [Ca(2+)]i, further research may demonstrate a correlation between normalization of [Ca(2+)]i and response to one of these medications, and further research may clarify whether a subgroup of patients may respond well to calcium channel antagonists.