Contribution of delayed rectifier potassium currents to the electrical activity of murine colonic smooth muscle

We used intracellular microelectrodes to record the membrane potential ( V m ) of intact murine colonic smooth muscle. Electrical activity consisted of spike complexes separated by quiescent periods ( V m ≈−60 mV). The spike complexes consisted of about a dozen action potentials of approximately 30 mV amplitude. Tetraethylammonium (TEA, 1–10 mM) had little effect on the quiescent periods but increased the amplitude of the action potential spikes. 4-Aminopyridine (4-AP, ⋧ 5 mM) caused continuous spiking. Voltage clamp of isolated myocytes identified delayed rectifier K + currents that activated rapidly (time to half-maximum current, 11.5 ms at 0 mV) and inactivated in two phases (τ f = 96 ms, τ s = 1.5 s at 0 mV). The half-activation voltage of the permeability was −27 mV, with significant activation at −50 mV. TEA (10 mM) reduced the outward current at potentials positive to 0 mV. 4-AP (5 mM) reduced the early current but increased outward current at later times (100–500 ms) consistent with block of resting channels relieved by depolarization. 4-AP inhibited outward current at potentials negative to −20 mV, potentials where TEA had no effect. Qualitative PCR amplification of mRNA identified transcripts encoding delayed rectifier K + channel subunits Kv1.6, Kv4.1, Kv4.2, Kv4.3 and the Kvβ1.1 subunit in murine colon myocytes. mRNA encoding Kv 1.4 was not detected. We find that TEA-sensitive delayed rectifier currents are important determinants of action potential amplitude but not rhythmicity. Delayed rectifier currents sensitive to 4-AP are important determinants of rhythmicity but not action potential amplitude.