The effects of exposure of hippocampal and dorsal root ganglion neurons of rats to a 2.45 GHz electromagnetic field (WLAN) on TRPV1 ion channel activity, oxidative stress and apoptosis in association with epilepsy should be investigated.
In the study, two different types of cells were extracted from rats and divided into the following groups: a) groups using hippocampal neurons: 1) from healthy rats (n=10) (control group), 2) from epileptic rats (n=8 or 10?), 3) exposed neurons from epileptic rats (n=8 or 10?), 4) exposed neurons from epileptic rats (n=8 or 10?) and addition of capsazepine.
b) groups using dorsal root ganglion neurons: 5) from healthy rats (n=8) (control group), 6) treatment with capsaicin (from 6 rats), 7) exposed neurons (from 6 rats), 8) exposed neurons (from 6 rats) and addition of capsaicin plus capsazepine after 1 hour, 9) treatment with different calcium channel inhibitors (from 6 rats), 10) exposed neurons and treatment with different calcium channel inhibitors (from 6 rats).
TRPV1 is a calcium-permeable and non-selective ion channel, gated by noxious heat, oxidative stress and capsaicin. To induce epilepsy, pentylenetetrazol was administered to rats. Capsaicin was used to activate TRPV1 ion channels while capsazepine was used as a capsaicin antagonist to block TRPV1.
|Exposure duration||continuous for 1 hour|
|Distance between exposed object and exposure source||25 cm|
|Chamber||exposure system was kept in a specific room which included plastic furniture and the walls of the room were covered by chromium-nickel plates (diameter: 1 mm) for shielding against environmental EMF|
|Setup||cells were kept in 15 ml Falcon tubes placed in a non-conductive plexi glass table in a circulatory water bath next to the antenna; temperature in room and in tubes was maintained at 37°C (relative humidity of 83 %)|
The free intracellular calcium, oxidative stress, apoptosis, mitochondrial membrane depolarization and the enzyme activities of caspase-3 and -9 were significantly increased while cell viability was significantly decreased in epileptic rat hippocampus neurons (group 2) compared to the control group. Additional WLAN exposure (group 3) induced a further intracellular calcium increase, while a treatment of the neurons with capsazepine (group 4) resulted in a protection against epilepsy-induced calcium influx, apoptosis and oxidative stress.
The test on TRPV1 ion channel activity in WLAN exposed and non-exposed dorsal root ganglion neurons and treatment with calcium channel inhibitors (group 10) indicated that WLAN exposure induced calcium influx via the TRPV1 channels.
The authors conclude that exposure of hippocampal and dorsal root ganglion neurons of rats to a 2.45 GHz electromagnetic field (WLAN) and epilepsy could induce a calcium influx in cells via TRPV1 ion channels, oxidative stress and apoptosis and that capsazepine might attenuate these effects.