ArticleMetabolic brain disease2014
Electromagnetic radiation (Wi-Fi) and epilepsy induce calcium entry and apoptosis through activation of TRPV1 channel in hippocampus and dorsal root ganglion of rats.
Article in Metabolic brain disease, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 63 citations in OpenAlex.
- Ultra short waves alleviate ulcerative colitis via TRPV2 mediated-macrophage polarization.iScience · 2026Article
- Effects of seasonal factors on brain function: Systematic review and future perspectives.iScience · 2025Article
- Selenium reduces oxaliplatin induced neuropathic pain: focus on TRPV1.Frontiers in pharmacology · 2025Article
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- Toxic Peptide FromFrontiers in pharmacology · 2021Article
- Radiofrequency electromagnetic field affects heart rate variability in rabbits.Physiological research · 2020Article
- Calcium Entry through TRPV1: A Potential Target for the Regulation of Proliferation and Apoptosis in Cancerous and Healthy Cells.International journal of molecular sciences · 2020Review
- Pleiotropic Pharmacological Actions of Capsazepine, a Synthetic Analogue of Capsaicin, against Various Cancers and Inflammatory Diseases.Molecules (Basel, Switzerland) · 2019Review
- Inhibitions of anandamide transport and FAAH synthesis decrease apoptosis and oxidative stress through inhibition of TRPV1 channel in an in vitro seizure model.Molecular and cellular biochemistry · 2019Article
- Long term exposure to cell phone frequencies (900 and 1800 MHz) induces apoptosis, mitochondrial oxidative stress and TRPV1 channel activation in the hippocampus and dorsal root ganglion of rats.Metabolic brain disease · 2018Article
- Effect of Microwave Wi-Fi Radiation at Frequency of 2.4 GHz on Epileptic Behavior of Rats.Journal of biomedical physics & engineering · 2018Article
- The effect of Wi-Fi electromagnetic waves in unimodal and multimodal object recognition tasks in male rats.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2017Article
- Diabetes enhances oxidative stress-induced TRPM2 channel activity and its control by N-acetylcysteine in rat dorsal root ganglion and brain.Metabolic brain disease · 2016Article
- Increased Expression of Transient Receptor Potential Vanilloid 4 in Cortical Lesions of Patients with Focal Cortical Dysplasia.CNS neuroscience & therapeutics · 2016Article
- Molecular Targets of Cannabidiol in Neurological Disorders.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2015Review
- Blockade of transient receptor potential cation channel subfamily V member 1 promotes regeneration after sciatic nerve injury.Neural regeneration research · 2015Article
- Epilepsy but not mobile phone frequency (900 MHz) induces apoptosis and calcium entry in hippocampus of epileptic rat: involvement of TRPV1 channels.The Journal of membrane biology · 2015Article
- Reduction in traumatic brain injury-induced oxidative stress, apoptosis, and calcium entry in rat hippocampus by melatonin: Possible involvement of TRPM2 channels.Metabolic brain disease · 2015Article
- Psychiatric Disorders and TRP Channels: Focus on Psychotropic Drugs.Current neuropharmacology · 2015Review
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Authors and funding
2 authors at 1 institution in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
Incidence rates of epilepsy and use of Wi-Fi worldwide have been increasing. TRPV1 is a Ca(2+) 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 Ca(2+) entry through activation of TRPV1 channel in epilepsy. Therefore, we tested the effects of Wi-Fi (2.45 GHz) exposure on Ca(2+) 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 Ca(2+), 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 Ca(2+) increase. However, pretreatment of the neurons with CPZ, results in a protection against epilepsy-induced Ca(2+) influx, apoptosis and oxidative damages. In results of whole cell patch-clamp experiments, treatment of DRG with Ca(2+) channel antagonists [thapsigargin, verapamil + diltiazem, 2-APB, MK-801] indicated that Wi-Fi exposure induced Ca(2+) influx via the TRPV1 channels. In conclusion, epilepsy and Wi-Fi in our experimental model is involved in Ca(2+) 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.
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