Fig. 5: POm-mediated DSDPs are due to the closing of K2P channels.

a Dendritic recordings of a BT neuron held at different holding potentials during the photostimulation of POm afferents (5 pulses of 5 ms at 8 Hz, every 10 s). At a holding potential of −60 mV, DSDPs appear as long-lasting depolarizing events (gray patches). At a holding potential of −125 mV the DSDPs became hyperpolarizing events. b DSDP amplitude evoked by the stimulation of POm as a function of the holding potential (n \(=\) 6 neurons, from 5 mice). The reversing potential of these events was measured at −94 mV consistent with a potassium conductance (see Methods). Error bars indicate s.e.m. c Dendritic recordings of a BT neuron during the stimulation of POm afferents (5 pulses of 1 ms at 8 Hz, every 10 s) before and after bath application of bupivacaine (1 mM), QX-314 (1 mM) and barium (1 mM). No DSDPs could be observed in the presence of this non-specific blockade of K2P channels. d DSDPs frequency was significantly reduced in the presence of non-specific K2P channels blockers (n \(=\) 3, from 3 mice, P \(=\) 0.023, two-sided paired t-test). e The selective blockade of TASK or TREK channels using A1899 (100 nM) or fluoxetine (100 µM) respectively, largely prevented the generation of DSDPs (for A1899, n \(=\) 4, from 3 mice, P \(=\) 0.001; for fluoxetine, n \(=\) 4, from 3 mice, P \(=\) 0.018, two-sided paired t-tests). f Altogether, the K2P blockers used in (d, e) significantly increase the membrane resistance of the recorded dendrites (control: 88.5 ± 15.9 MΩ, with blockers: 111.3 ± 16.6 MΩ, n \(=\) 11, from 3 mice, P \(=\) 0.004, two-sided paired t-test). g Blocking the THIK channel family with IBMX (1 mM) did not produce any change in the frequency of DSDPs (n \(=\) 4, from 3 mice, P \(=\) 0.62, two-sided paired t-test). Source data are provided as a Source Data file.