Topic: GABAB receptors

Aim: We explored the role of the GABAB auxiliary subunit KCTD16 in nociceptive synaptic transmission in naïve mice and in model of peripheral inflammation.Methods: KCTD16 -/- KO mice (obtained from B. Bettler, Uni Basel) WT and the transgenic mice (VGAT-ChR2-EYFP crossed with KCTD16 KO) were used. Behavioral testing of mechanical (von Frey filament) and thermal (hot plate) sensitivity, patch clamp recordings from dorsal horn neurons in spinal cord slices (miniature postsynaptic excitatory currents mEPSC, light evoked inhibitory currents leIPSC) were used. Inflammation was induced by intraplant

P50 suppression is a sensory gating phenomenon where the EEG response to the second out of two auditory clicks is decreased in amplitude. Clinical studies have reported the magnitude of P50 suppression to be impaired in schizophrenia. Here, we used a network model of multicompartmental neurons to explore the mechanisms of P50 suppression deficits in schizophrenia. The model consisted of a population of pyramidal neurons interconnected with two interneuron populations: large basket cells and neurogliaform cells, where the latter activates GABAB-receptor mediated post-synaptic currents in its ta