Voltage- and calcium-activated potassium currents in mouse neuroblastoma x rat glioma hybrid cells.
1. Membrane currents were recorded from voltage-clamped, microelectrode-impaled cells of the NG108-15 mouse neuroblastoma x rat glioma clonal cell line, differentiated with prostaglandin E1. 2. A slow outward tail current reversing at post-pulse potentials between -80 and -90 mV was evoked by depolarizing pre-pulses to near 0 mV. The tail current was inhibited by Cd2+ ions (0.2-1 mM) and hence attributed to activation of a Ca2+-dependent K+ current by a priming voltage-activated Ca2+ current. 3. Two components to this tail current could be distinguished pharmacologically: an early (less than or equal to 50 ms) component inhibited by 1-5 mM-tetraethylammonium (TEA), and a late component lasting several hundred milliseconds inhibited by apamin (0.1-0.4 microM) or d-tubocurarine (0.1-0.5 mM). 4. Ionophoretic injection of Ca2+ ions evoked a transient outward current with an apparent reversal potential (from ramped current-voltage curves) of -70 mV. This current was succeeded or sometimes replaced by an inward current with an apparent reversal potential between -20 and -10 mV. 5. The outward current induced by Ca2+ injections was unaffected or partly inhibited by TEA (1-5 mM), but was strongly inhibited by apamin or d-tubocurarine. 6. Hyperpolarizing voltage steps from between -30 and -40 mV induced inward current relaxations reversing at between -80 and -90 mV. These were considered to result from deactivation of the voltage-dependent sustained K+ current, IM. 7. Application of methacholine, muscarine or Ba2+ ions produced an inward current, reduced input conductance and reduced IM deactivation relaxations. 8. It is concluded that differentiated NG108-15 cells possess several of the K+ currents present in sympathetic neurones, including a delayed rectifier current, two species of Ca2+-activated K+ current and the M-current.
Brown
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Laboratory of Cell Biology, National Institute of Mental Health, Bethesda, MD 20892.
Higashida
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D000200:Action Potentials / Q000187:drug effects; D000818:Animals; D001464:Barium / Q000494:pharmacology; D002104:Cadmium / Q000494:pharmacology; D002118:Calcium / Q000494:pharmacology*; D002460:Cell Line; D003035:Cobalt / Q000494:pharmacology; D006822:Hybrid Cells / Q000502:physiology*; D007473:Ion Channels / Q000502:physiology*; D016210:Methacholine Chloride; D008688:Methacholine Compounds / Q000494:pharmacology; D051379:Mice; D011188:Potassium / Q000502:physiology*; D051381:Rats; D019789:Tetraethylammonium; D013757:Tetraethylammonium Compounds / Q000494:pharmacology; D014403:Tubocurarine / Q000494:pharmacology
D007473:Ion Channels; D008688:Methacholine Compounds; D013757:Tetraethylammonium Compounds; D002104:Cadmium; D016210:Methacholine Chloride; D001464:Barium; D003035:Cobalt; D019789:Tetraethylammonium; D011188:Potassium; D002118:Calcium; D014403:Tubocurarine