Celon Pharma Ltd, Ogrodowa 2a, 05-092 Lomianki, Poland.
Prog Neuropsychopharmacol Biol Psychiatry. 2010 Dec 1;34(8):1367-74. doi: 10.1016/j.pnpbp.2010.08.020. Epub 2010 Sep 8.
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.
精神分裂症的发病机制涉及几个复杂的细胞机制，目前还不完全清楚。最近的研究表明，包括多巴胺能和谷氨酸能神经递质传递改变在内的疾病的主要特征性原发性紊乱，以及神经元钙（Ca（2+））内稳态和信号传导受损之间存在关联。新兴的 Ca（2+）假说将参与精神分裂症发病机制的各种细胞过程联系起来并统一起来，并表明 Ca（2+）内稳态失调在疾病的病因学中起着核心作用。这篇综述探讨了精神分裂症中 Ca（2+）内稳态和信号转导的体外数据。这项研究的主要限制是缺乏精神分裂症标志物和经过验证的疾病模型。正如本综述所指出的，克服这些限制的一种方法可能是分析精神分裂症患者外周细胞中的 Ca（2+）信号体。精神分裂症动物模型的验证可能允许在活体动物中应用先进的 Ca（2+）成像技术。
