| Article ID | Journal | Published Year | Pages | File Type |
|---|---|---|---|---|
| 2565133 | Progress in Neuro-Psychopharmacology and Biological Psychiatry | 2010 | 8 Pages |
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 (Ca2+) homeostasis and signaling. Emerging Ca2+ hypothesis links and unifies various cellular processes involved in the pathogenesis of schizophrenia and suggests a central role of dysregulation of Ca2+ homeostasis in the etiology of the disease. This review explores the in vitro data on Ca2+ 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 Ca2+ signalosomes in peripheral cells from schizophrenia patients. Validation of animal models of schizophrenia may permit the application of advanced Ca2+ imaging techniques in living animals.
