Abstract:

An accumulating body of evidence indicates that abnormalities of intracellular free calcium ([Ca2+]i) concentration is caused by excessive levels of reactive oxygen species (ROS) in rats with cerebral ischemia in play an important role in the pathophysiology of cerebral ischemia (Miyanohara et al. 2015 Belrose and Jackson, 2018). Ca2+ passes cell membrane via different channels such as chemical and voltage gated channels. Apart from the well-known cation channels, there is recently discovered channels namely transient receptor potential (TRP) family. The TRP superfamily is containing 7 subfamilies with 28 members in mammalian. Activation and inhibition mechanisms of the TRP channels are very different from the voltage gated calcium channels. For example, TRPM2 channel is activated by ADP-ribose and oxidative stress, but TRPV1 channel is activated several stimuli, including capsaicin and oxidative stress (Belrose and Jackson, 2018). Dexmedetomidine (DEX) is an important drug for long-term sedation in intensive care patients because it induces a rapid response and is easily controllable. There is some modulator role of DEX on the [Ca2+]i concentration in several neurons (Akpınar et al. 2016).  Results of a recent study indicated that DEX induced modulator role on cerebral ischemia-induced ROS, TRPM2 and TRPV1 channel activation in hippocampusof rats. I concluded that the results of recent studies suggest that DEX treatment reduces cerebral ischemiainduced oxidative stress and intracellular Ca2+ signaling through inhibition of TRP channels. It seems to that the exact relationship between TRP channel activation and DEX in cerebral ischemia still remains to be determined.

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