Disruption of Calcium Homeostasis and Following Changes in Calcium Signaling in Neurons and Glial Cells in Response to Photodynamic Treatment

Abstract

Photodynamic impact on neurons and glial cells, causing oxidative stress and ischemic damage, is accompanied by disruption of calcium homeostasis and activation or suppression of diverse calcium-dependent mechanisms, such as calcium pumps and channels, calcium-dependent signaling or executive proteins, and other signaling systems that interact with calcium pathway, like ion channels, pumps and exchangers, nitric oxide, glutamate, and others. The cascade of processes initiated by oxidative stress and ischemia in nervous tissue, includes both protective responses and apoptotic or necrotic cell death scenarios. This mini review surveys the publications on these processes and compares them with the data obtained in our laboratory on the model of photothrombotic stroke on rat brain in vivo and the model of photodynamic treatment on crayfish mechanoreceptor in vitro. These areas of research are driven by the need to find methods of emergency neuroprotection in ischemic stroke and to improve the accuracy and efficiency of photodynamic therapy of tumors with minimized damage to benign tissues. A proteomic study of the penumbra region in the photothrombotic stroke model revealed changes in the expression of a number of calcium-dependent proteins associated with impaired calcium homeostasis and having either a protective or damaging tendency. Inhibitory analysis of the effects of photo-oxidative stress on the crayfish stretch receptor model revealed the involvement of a number of proteins in the calcium-dependent pathway in neuronal or glial cell death or survival. In this paper, these data are analyzed and summarized to identify promising directions for further research.