Voltage- and calcium-activated potassium currents in mouse neuroblastoma x rat glioma hybrid cells

• Published in: The Journal of physiology Vol. 397; no. 1; pp. 149 - 165
• Main Authors: Brown, D A, Higashida, H
• Format: Journal Article
• Language: English
• Published: England The Physiological Society 01-03-1988
• Subjects: Action Potentials - drug effects; Animals; Barium - pharmacology; Cadmium - pharmacology; calcium; Calcium - pharmacology; Cell Line; Cobalt - pharmacology; Hybrid Cells - physiology; Ion Channels - physiology; Methacholine Chloride; Methacholine Compounds - pharmacology; Mice; neuroblastoma cells; potassium; Potassium - physiology; Rats; Rodentia; Tetraethylammonium; Tetraethylammonium Compounds - pharmacology; Tubocurarine - pharmacology
• ISSN: 0022-3751; 1469-7793
• DOI: 10.1113/jphysiol.1988.sp016993

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.