TRPV1 channel is a potential drug discovery channel for epilepsy

Abstract

Epilepsy is one of the most frequent and  heterogeneous neurological disorders and it is  characterized by several disabilities. Epilepsy is  affecting about 3% of people worldwide. Current antiepileptic  drugs are only effective in 60% of individuals  and many drugs can induce several unwanted side  effects in patients. Etiology of epilepsy has not been  clarified fully. However, increased intracellular calcium  ion (Ca 2+ ) concentration has main role in etiology of  epilepsy. Ca2+ passes the cell membrane through  different cell membrane channels. One of the channels  is TRP superfamily. The family is containing six  subfamilies. TRPV1 channel is a member of TRPV  subfamily. Capsaicin is a component of hot chili pepper.  The TRPV1 channels is activated by different stimuli  such as acidic pH, high temperature (≥ 42° C) and  capsaicin, causing pain, inflammation and hyperalgesia  in peripheral nervous system (Caterina et al. 1997). Is  has been well known that hippocampus is main area in  the brain for induction of epilepsy. Expression levels of  TRPV1 channels in different areas of hippocampus are  high (Gonzalez-Reyes et al. 2013). Results of recent  studies indicated involvement of TRPV1 channels in  epilepsy (Naziroglu and Ovey, 2015; Cho et al. 2018).  In the oral presentation, I discussed novel roles of  TRPV1 on the epilepsy induction by the capsaicin.  Results of a recent study indicated increased levels  of intracellular Ca2+ concentration in hippocampus of  epilepsy induced rats (Naziroglu and Ovey, 2015).  They also observed increased levels of intracellular  mitochondrial oxidative stress and apoptosis levels in  the neurons by the capsaicin stimulation. However, their  levels were decreased by inhibition of TRPV1 channel  blocker, capsazepine.  I concluded that the results of recent studies  suggest that TRPV1 stimulation through capsaicin  causes oxidative stress and  intracellular Ca2+ signaling  in epileptic rats. It seems to that the certain role of  TRPV1 channel activation in in the epilepsy still  remains to be determined.