Figure 4. Pharmacological characterisation of the background K⁺ current in cultured GPN neurones.

A-C, traces showing representative examples of the effect of hypoxia (A), halothane (B) and arachidonic acid (AA) (C) on the background current elicited during ramp depolarisation from −100 to +25 mV. Holding potential was −60 mV. Note the reversible inhibition of the current by hypoxia in A, and by halothane (2–5 mm) in B. In the presence of halothane, hypoxia produces no further inhibition of the current (B). In contrast, 5 μm AA potentiated the background current in C, and appeared to occlude the hypoxic response. D, effect of several agents on the background current in normoxia and hypoxia under symmetrical K⁺ conditions; for each agent bars represent the difference current at −60 mV expressed as a percentage of the control current (in normoxia); the difference current was obtained by subtracting the current during the particular treatment from the control current. The effects of hypoxia (Hox), halothane (Hal, 2–5 mm), quinidine (Quid, 1 mm) and barium (Ba²⁺, 10 mm) were all inhibitory. Note, however, that AA (5 μm) caused potentiation of the background current. In addition, when halothane and Ba²⁺ were applied in combination with hypoxia (Hal + Hox; Ba²⁺+ Hox) there was occlusion of the response to hypoxia (P < 0.05). I_K,O2 was also occluded in presence of 1 mm quinidine (Quid), which completely inhibited the background current. The sample size n is indicated in parentheses within the bars; ^*P < 0.05.