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Potassium currents in adult rat intracardiac neurones.
Author(s) -
XiMoy S X,
Dun N J
Publication year - 1995
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.1995.sp020787
Subject(s) - chemistry , hyperpolarization (physics) , cardiac transient outward potassium current , time constant , membrane potential , repolarization , muscarine , reversal potential , inward rectifier potassium ion channel , resting potential , electrophysiology , depolarization , biophysics , relaxation (psychology) , patch clamp , analytical chemistry (journal) , ion channel , medicine , stereochemistry , biochemistry , chromatography , muscarinic acetylcholine receptor , receptor , nuclear magnetic resonance spectroscopy , electrical engineering , biology , engineering
1. Properties of K+ currents were studied in isolated adult rat parasympathetic intracardiac neurones with the use of single‐electrode voltage‐clamp techniques. 2. A hyperpolarization‐activated inward rectifier current was revealed when the membrane was clamped close to the resting level (‐60 mV). The slowly developing inward relaxation had a mean amplitude of 450 pA at ‐150 mV, an activation threshold of ‐60 to ‐70 mV and a relaxation time constant of 41 ms at ‐120 mV. The current was reversibly blocked by Cs+ (1 mM) and became smaller with reduced [K+]o and [Na+]o, indicating that this inward rectifier current probably is a time‐ and voltage‐dependent Na(+)‐K+ current. 3. Step depolarizations from the holding potential of ‐80 mV evoked a transient (< 100 ms at ‐40 mV) outward K+ current (IA) which was blocked by 4‐aminopyridine (4‐AP, 1 mM). The time constants for IA inactivation were 20 ms at ‐50 mV and 16 ms at ‐20 mV. The steady‐state activation and (removal of) inactivation curve showed a small overlap between ‐70 and ‐40 mV; the reversal potential of IA was close to EK. 4. Step hyperpolarizations from the depolarized potentials, i.e. ‐30 mV, revealed a slow inward relaxation associated with the deactivation of a time‐ and voltage‐dependent current. The inward relaxation became faster at more hyperpolarized potentials and reversed at ‐85 and ‐53 mV in 4.7 and 15 mM [K+]o. This current was blocked by muscarine (20 microM) and Ba2+ (1 mM) but not affected by Cs+ (1 mM); this current may correspond to the M‐current (IM). 5. Depolarization‐activated outward K+ currents were evoked by holding the membrane close to the resting potential in the presence of tetrodotoxin (TTX, 3 microM), 4‐AP (1 mM) and Ba2+ (1 mM). The amplitude of the outward relaxation and the tail current became smaller as the [K+]o was elevated. The outward tail current was reduced in a Ca(2+)‐free solution and the residual current was eliminated by the addition of tetraethylammonium (TEA, 10 mM); the reversal potential was shifted in a direction predicted by the Nernst equation. These findings suggest the presence of delayed rectifier K+ current and Ca(2+)‐activated K+ current. 6. Superfusion of TEA, Ba2+ and 4‐AP, but not Cs+, induced rhythmic discharges in some of the otherwise quiescent intracardiac neurones.(ABSTRACT TRUNCATED AT 400 WORDS)