Slowly inactivating potassium current in cultured bull-frog primary afferent and sympathetic neurones.
1. Cultured bull-frog dorsal root ganglion cells were voltage clamped in the whole-cell configuration. The cells were superfused with a nominally calcium-free Ringer solution containing tetrodotoxin (3 microM), magnesium (10 mM), cobalt (1 mM), barium (2 mM), 4-aminopyridine (3 mM) and caesium (2 mM). 2. Step depolarizations (10-40 mV, 100-300 ms) from a holding potential close to the rest (typically -70 mV) evoked an outward current (IK) followed by an outward tail current. The peak amplitude of the current was reduced to less than 10% by tetraethylammonium (30 mM). 3. IK developed to its peak in 200 ms at -30 mV. Tail currents reversed at potentials that changed according to the logarithm of the extracellular potassium concentrations. 4. Tail currents declined to the baseline according to an exponential function of time (tau congruent to 40 ms at -60 mV) and its reciprocal time constant increased e-fold with a 13 mV hyperpolarization. 5. The current inactivated during sustained (1-20 s) depolarizing pulses according to a single exponential function (tau congruent to 3 s). 6. The peak amplitude of IK at -30 mV was progressively increased as the holding potential was made more negative than -70 mV reaching the maximum with step depolarizations from -120 mV. Reversed phenomenon was observed as the holding potential was made less negative than -70 mV. 7. The removal of the steady-state inactivation occurred along with a single exponential function and the time constant was decreased from 70 ms at -70 mV to 10 ms at -120 mV. 8. It is suggested that a slowly inactivating potassium current which we called IK in amphibian sensory neurones could be a class of a 'delayed' rectifier potassium current. A potassium current with properties indistinguishable from those which have been described for the sensory IK also occurred in cultured bull-frog sympathetic neurones. 9. Forskolin (1-30 microM) and 1,9-dideoxy forskolin (10 microM) reduced the amplitude of IK by up to 85% but these actions were not mimicked by any of 8-bromo-cyclic AMP (1 mM), dibutyryl cyclic AMP (1 mM) and 3-isobutyl-1-methylxanthine (1 mM). A hydrophilic forskolin analogue, 7-O-hemisuccinyl-7-deacetyl forskolin (10 microM), was about one-tenth as potent as forskolin (10 microM).
Tokimasa
T
T
Department of Physiology, Kurume University School of Medicine, Japan.
Tsurusaki
M
M
Akasu
T
T
D000818:Animals; D002478:Cells, Cultured; D005576:Colforsin / Q000494:pharmacology; D004594:Electrophysiology; D007700:Kinetics; D008564:Membrane Potentials / Q000502:physiology; D009474:Neurons / Q000378:metabolism*; D009475:Neurons, Afferent / Q000378:metabolism; D011188:Potassium / Q000378:metabolism*; D015221:Potassium Channels / Q000187:drug effects; D011892:Rana catesbeiana; D013564:Sympathetic Nervous System / Q000378:metabolism*; D019789:Tetraethylammonium; D013757:Tetraethylammonium Compounds / Q000494:pharmacology
D015221:Potassium Channels; D013757:Tetraethylammonium Compounds; D005576:Colforsin; D019789:Tetraethylammonium; D011188:Potassium