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The erg inwardly rectifying K + current and its modulation by thyrotrophin‐releasing hormone in giant clonal rat anterior pituitary cells
Author(s) -
Bauer Christiane K.
Publication year - 1998
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 - 10.1111/j.1469-7793.1998.063bz.x
Subject(s) - depolarization , membrane potential , chemistry , resting potential , endocrinology , biophysics , medicine , repolarization , hyperpolarization (physics) , electrophysiology , stereochemistry , biology , biochemistry , nuclear magnetic resonance spectroscopy
1 The voltage‐dependent inwardly rectifying K + current ( I K,IR ) of clonal rat anterior pituitary cells (GH 3 /B 6 ) was investigated in solutions with physiological K + gradient using giant polynuclear cells. 2 IK,IR was isolated by the use of the selective erg ( ether‐à‐go‐go ‐related gene) channel blocker E‐4031. In external 5 mM K + solution, I K,IR carried steady‐state outward current in the potential range between –60 and 0 mV, with a maximum current amplitude at –40 mV. Negative to the K + equilibrium potential, E K , large transient inward currents occurred. 3 A selective pharmacological block of I K,IR induced a sustained depolarization of the membrane potential when Ca 2+ action potentials were blocked, confirming the contribution of I K,IR to the resting membrane potential of GH 3 /B 6 cells. 4 Thyrotrophin‐releasing hormone (TRH) reduced effectively the sustained outward and the transient inward I K,IR . The magnitude of a TRH‐induced depolarization of the membrane potential was consistent with an almost complete reduction of I K,IR . 5 The results demonstrate that the TRH‐induced reduction of I K,IR is able to mediate the resting potential depolarization, suggesting that the increase in the frequency of action potentials occurring during the second phase of the TRH response in GH cells should be sustained by I K,IR inhibition. Moreover, this is the first evidence of a ligand‐induced physiological modulation of an erg‐mediated current.