Roles of dexmedetomidine and calcium signaling in cerebral ischemia: Focus TRP channels

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 (Akpinar 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 hippocampus of 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.