In vitro findings of alterations in intracellular calcium homeostasis in schizophrenia

Abstract

The pathogenesis of schizophrenia involves several complex cellular mechanisms and is not well understood. Recent research has demonstrated an association between primary disturbances characteristic of the disease, including altered dopaminergic and glutamatergic neurotransmission, and impairments in neuronal calcium (Ca(2+)) homeostasis and signaling. Emerging Ca(2+) hypothesis links and unifies various cellular processes involved in the pathogenesis of schizophrenia and suggests a central role of dysregulation of Ca(2+) homeostasis in the etiology of the disease. This review explores the in vitro data on Ca(2+) homeostasis and signaling in schizophrenia. Major limitation in this research is the lack of schizophrenia markers and validated disease models. As indicated in this review, one way to overcome these limitations may be analyses of Ca(2+) signalosomes in peripheral cells from schizophrenia patients. Validation of animal models of schizophrenia may permit the application of advanced Ca(2+) imaging techniques in living animals.