Electromagnetic radiation (Wi-Fi) and epilepsy induce calcium entry and apoptosis through activation of TRPV1 channel in hippocampus and dorsal root ganglion of rats
Incidence rates of epilepsy and use of Wi-Fi worldwide have been increasing. TRPV1 is a Ca2+ permeable and non-selective channel, gated by noxious heat, oxidative stress and capsaicin (CAP). The hyperthermia and oxidant effects of Wi-Fi may induce apoptosis and Ca2+ entry through activation of TRPV1 channel in epilepsy. Therefore, we tested the effects of Wi-Fi (2.45 GHz) exposure on Ca2+ influx, oxidative stress and apoptosis through TRPV1 channel in the murine dorsal root ganglion (DRG) and hippocampus of pentylentetrazol (PTZ)-induced epileptic rats. Rats in the present study were divided into two groups as controls and PTZ. The PTZ groups were divided into two subgroups namely PTZ + Wi-Fi and PTZ + Wi-Fi + capsazepine (CPZ). The hippocampal and DRG neurons were freshly isolated from the rats. The DRG and hippocampus in PTZ + Wi-Fi and PTZ + Wi-Fi + CPZ groups were exposed to Wi-Fi for 1 hour before CAP stimulation. The cytosolic free Ca2+, reactive oxygen species production, apoptosis, mitochondrial membrane depolarization, caspase-3 and −9 values in hippocampus were higher in the PTZ group than in the control although cell viability values decreased. The Wi-Fi exposure induced additional effects on the cytosolic Ca2+ increase. However, pretreatment of the neurons with CPZ, results in a protection against epilepsy-induced Ca2+ influx, apoptosis and oxidative damages. In results of whole cell patch-clamp experiments, treatment of DRG with Ca2+ channel antagonists [thapsigargin, verapamil + diltiazem, 2-APB, MK-801] indicated that Wi-Fi exposure induced Ca2+ influx via the TRPV1 channels. In conclusion, epilepsy and Wi-Fi in our experimental model is involved in Ca2+ influx and oxidative stress-induced hippocampal and DRG death through activation of TRPV1 channels, and negative modulation of this channel activity by CPZ pretreatment may account for the neuroprotective activity against oxidative stress.
KeywordsHippocampus Dorsal root ganglion Wi-Fi Epilepsy Apoptosis TRPV1 channel
Dorsal root ganglion
Reactive oxygen species
Transient receptor potential
Transient receptor potential vanilloid 1
Dr. Vahid Ghazizadeh was partially supported for the project by Free Oxygen Radical Society, Isparta, Turkey. Abstract of the manuscript submitted in 11th National Neuroscience Congress, April, 2013, Izmir, Turkey. The authors wish thanks to Dr. Peter Butterworth (King’s College London, UK) for revision of English of the manuscript. Authors’ roles: MN formulated the present hypothesis and was responsible for writing the report. VG were responsible for the analyses.
Conflict of interest
The authors declare that they have no conflict of interest. All authors approved the final manuscript.
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