Our study explores the role of the Potassium Channel Tetramerization Domain Containing Protein 16 (KCTD16), in modulation of nociceptive synaptic transmission and identified the auxiliary GABAB receptor (GABABR) as a key modulator involved. Using KCTD16 knockout (KO) mice, we combine behavioral, histological, and electrophysiological methods to uncover its function in pain pathways as KCTD16 is highly expressed in the spinal dorsal horn and dorsal root ganglia. Our findings reveal, for the first time, a functional link between KCTD16 and nociceptive synaptic modulation. The results suggest that disruption of the GABABR-KCTD16 complex weakens pre- and postsynaptic inhibition, contributing to altered pain processing. This work is done in collaboration with Dr. Turecek from Institute of Experimental Medicine, Czech Academy of Science.
