Fig. 5.

NO inhibits a TASK-like current in hypoglossal motoneurons. A: traces of holding current and conductance show that in Cs⁺ (2 mM) to block hyperpolarization-activated cyclic nucleotide-gated (HCN) channels and tetraethylammonium (TEA; 10 mM) and 4-aminopyridine (4-AP; 50 μM) to block voltage-gated K⁺ channels, exposure to DEA (20 μM) decreased outward current and conductance. B: average (n = 6) current-voltage (I-V) relationship of the NO-sensitive current (determined by subtracting I-V relationships obtained during exposure to DEA from those recorded in the absence of DEA) in Cs⁺ is similar to a TASK-like conductance, i.e., relatively voltage-independent current that is active at resting membrane potential and reverses near the equilibrium potential for K⁺. C: summary data (n = 6) show DEA-induced changes in holding current in Cs⁺ alone and in Cs⁺ with TEA and 4-AP. D: traces of holding current and conductance show that in Cs⁺, exposure to DEA decreased outward current and conductance. However, responsiveness to a second DEA exposure was reduced by methanandamide (Met; 10 μM), a TASK channel blocker. E1 and E2: average I-V relationships in Cs⁺ alone and during exposure to DEA in Cs⁺ with and without Met. F: summary data (n = 6) show that in the continued presence of Cs⁺, subsequent inhibition of TASK channels with Met decreased the DEA-induced change in holding current. *P < 0.05.