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Voltage‐ and calcium‐activated potassium currents in mouse neuroblastoma x rat glioma hybrid cells.
Author(s) -
Brown D A,
Higashida H
Publication year - 1988
Publication title -
the journal of physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.802
H-Index - 240
eISSN - 1469-7793
pISSN - 0022-3751
DOI - 10.1113/jphysiol.1988.sp016993
Subject(s) - apamin , chemistry , tetraethylammonium , cardiac transient outward potassium current , reversal potential , depolarization , biophysics , membrane potential , muscarine , 4 aminopyridine , potassium channel , potassium , patch clamp , biochemistry , biology , muscarinic acetylcholine receptor , receptor , organic chemistry
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.