Mechanical allodynia (pain to normally innocuous tactile stimuli) is a widespread symptom of inflammatory and neuropathic pain. Spinal or medullary dorsal horn (SDH or MDH) circuits mediating tactile sensation and pain need to interact in order to evoke mechanical allodynia. PKCγ-expressing (PKCγ⁺) interneurons and inhibitory controls within SDH/MDH inner lamina II (II_i) are pivotal in connecting touch and pain circuits. However, the relative contribution of GABA and glycine to PKCγ⁺ interneuron inhibition remains unknown. We characterized inhibitory inputs onto PKCγ⁺ interneurons by combining electrophysiology to record spontaneous and miniature IPSCs (sIPSCs, mIPSCs) and immunohistochemical detection of GABA_ARα2 and GlyRα1 subunits in adult rat MDH. While GlyR-only- and GABA_AR-only-mediated mIPSCs/sIPSCs are predominantly recorded from PKCγ⁺ interneurons, immunohistochemistry reveals that ~80% of their inhibitory synapses possess both GABA_ARα2 and GlyRα1. Moreover, nearly all inhibitory boutons at gephyrin-expressing synapses on these cells contain glutamate decarboxylase and are therefore GABAergic, with around half possessing the neuronal glycine transporter (GlyT2) and therefore being glycinergic. Thus, while GABA and glycine are presumably co-released and GABA_ARs and GlyRs are present at most inhibitory synapses on PKCγ⁺ interneurons, these interneurons exhibit almost exclusively GABA_AR-only and GlyR-only quantal postsynaptic inhibitory currents, suggesting a pharmacological specialization of their inhibitory synapses.

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.