The dorsal vagal nucleus expresses high levels of mRNA for the two-pore-domain K⁺ channels TASK-1 and TASK-3 in rodents [1,2]. We have previously demonstrated that rat dorsal vagal neurones (DVN) express functional TASK-1-containing K⁺ channels that are inhibited by 5-HT and modulated by pH_o changes [3]. Here we investigate their role in murine DVN using a recently developed TASK-1 KO mouse model [2]. Brainstem slices (200 μm) were obtained from wild-type (WT; juvenile and adult) and TASK-1 KO (adult) C57Bl6 mice. Following recovery at 34°C for 60 min, slices were maintained in standard NaHCO₃-buffered ACSF at RT. Whole-cell recordings were established using borosilicate glass electrodes (3-6 MΩ, filled with (in mM) 120 K-gluconate, 1 NaOH, 1 MgCl₂, 1 CaCl₂, 10 HEPES, 5 BAPTA, 2 K₂ATP, pH 7.3. Recordings were performed in HEPES-buffered ACSF [3]. Solutions of halothane were made up as fractions of a saturated solution at room temperature. The concentration of the saturated solution was taken to be 17.5 mM. Reservoirs containing the halothane solutions were sealed with a rigid plastic float, and all tubing and valves were made of polytetrafluoroethylene. All values are given as mean ± 1 s.e.m. DVN from juvenile WT mice had a resting potential (E_m) of -62±3 mV (n=16) and 56% were spontaneously active. DVN from adult mice had an E_m of -72±3 mV (n=14) and were not spontaneously active. The holding current at -20 mV (I_H-20) was 63±8 pA (n=14) for juvenile and 85±8 pA (n=28) for adult DVN. E_m and I_H-20 were not significantly different between adult WT and TASK-1 KO DVN. I_H-20 of both WT and KO was unaffected by ZnCl₂ (100 μM; n=4 each), suggesting the absence of homomeric TASK-3 channels. Next we investigated the pH-sensitivity of I_H-20. Consistent with a role for TASK-1, acidification (pH 6.3) reduced I_H-20 by 70±26 pA in WT. The underlying current had a reversal potential of -94±1 mV and was well described by the Goldman-Hodgkin-Katz (GHK) equation (n=5). In contrast, this current was not observed in TASK-1 KO (n=9). Raising pH from 7.3 to 8.5 elicited an outward current of 165±28 pA (n=10) in WT and 167±50 pA (n=4) in TASK-1 KO. However, the reversal potential of this current was -72±4 mV and -71±4 mV, respectively, and the current did not follow the GHK equation. The volatile anaesthetic halothane (1 mM), a known activator of TASK, elicited an outward current at -20 mV in 9 and an inward current in 2 out of 16 WT DVN. In contrast, only an inward current (4/7) or no response to halothane was seen in TASK-1 KO DVN. In agreement with our previous study in rat [3], the present data show that mice express functional acid-sensitive TASK-1-containing channels in DVN and that these are activated by halothane. Deletion of TASK-1 removes these channels, but no homomeric TASK-3 channels are observed [2]. In contrast to rat, mouse DVN exhibit an additional alkalinisation-induced outward current other than TASK.