Premium
A calcium‐activated potassium current in motor nerve terminals of the mouse.
Author(s) -
Mallart A
Publication year - 1985
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.1985.sp015877
Subject(s) - tetraethylammonium , chemistry , 4 aminopyridine , biophysics , cardiac transient outward potassium current , calcium , potassium , potassium channel , anatomy , patch clamp , biochemistry , biology , receptor , organic chemistry
Local circuit currents involving presynaptic terminals were recorded by micro‐electrodes inserted into the perineurium of nerves from the triangularis sterni muscle of the mouse. A transient outward current component was isolated by blocking the voltage‐activated (delayed rectifier) K current by 3,4‐diaminopyridine (3,4‐DAP). The amplitude of this component depended on external K concentration and fell to zero at [K]o = 15 mM. Since it also depended on [Ca]o, it was identified as a Ca‐activated K current (IK(Ca)). Tetraethylammonium (TEA) (2 mM), Ba (2 mM), Co (10 mM) and Mn (2.5 mM) blocked IK(Ca). IK(Ca) decayed to zero in approximately 12 ms and recovered from inactivation in about 100 ms. Ca current was enhanced in inverse proportion to the degree of IK(Ca) depression. The possible role of IK(Ca) in the process of neuromuscular facilitation is briefly discussed.