Dosimetry of Microelectrodes Array Chips for Electrophysiological Studies Under Simultaneous Radio Frequency Exposures

Studying the response of neuronal networks to radio frequency (RF) signals requires the use of a specific device capable of accessing and simultaneously recording neuronal activity during electromagnetic fields (EMF) exposure. In this study, a microelectrode array (MEA) that records the spontaneous activity of neurons is coupled to an open transverse electromagnetic (TEM) cell that propagates EMF. We characterize this system both numerically and experimentally at 1.8 GHz. Two MEA versions were compared, for the first time, to determine the impact of their design dissimilarities on the response to EMF. Macroscopic and microscopic measurements using, respectively, a fiber-optic probe and a temperature-dependent fluorescent dye (Rhodamine-B) were carried out. Results indicate that one MEA shows more stability toward the changes of the surrounding environment compared to the other MEA. Using a fiber-optic thermometer, the measured specific absorption rate (SAR) probe value in the center of the more stable MEA was 5.5 ± 2.3 W/kg. Using a Rhod-B microdosimetry technique, the measured SAR value at the level of the MEA electrodes was 7.0 ± 1.04 W/kg. SAR values are normalized per 1 W incident power. Due to the additional metallic planes and a smaller chip aperture, this new recording chip is steadier in terms of SAR and temperature stability allowing high exposure homogeneity as required during biological experiments. A typical neuronal activity recording under EMF exposure is reported

Comparative study between radiofrequency-induced and muscimol-induced inhibition of cul-3 tured networks of cortical neuron

Previous studies have shown that spontaneously active cultured networks of cortical neuron grown planar microelectrode arrays are sensitive to radiofrequency (RF) fields and exhibit an inhibitory response more pronounced as the exposure time and power increase. To better understand the mechanism behind the observed effects, we aimed at identifying similarities and differences between the inhibitory effect of RF fields (continuous wave, 1800 MHz) to the γ-aminobutyric acid type A (GABAA) receptor agonist muscimol (MU). Inhibition of the network bursting activity in response to RF exposure became apparent at an SAR level of 28.6 W/kg and co-occurred with an elevation of the culture medium temperature of ~1 °C. Exposure to RF fields preferentially inhibits bursting over spiking activity and exerts fewer constraints on neural network bursting synchrony, differentiating it from a pharmacological inhibition with MU. Network rebound excitation, a phenomenon relying on the intrinsic properties of cortical neurons, was observed following the removal of tonic hyperpolarization after washout of MU but not in response to cessation of RF exposure. This implies that hyperpolarization is not the main driving force mediating the inhibitory effects of RF fields. At the level of single neurons, network inhibition induced by MU and RF fields occurred with reduced action potential (AP) half-width. As changes in AP waveform strongly influence efficacy of synaptic transmission, the narrowing effect on AP seen under RF exposure might contribute to reducing network bursting activity. By pointing only to a partial overlap between the inhibitory hallmarks of these two forms of inhibition, our data suggest that the inhibitory mechanisms of the action of RF fields differ from the ones mediated by the activation of GABAA receptors