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Isolation of a long-lasting eag-related gene-type K+ current in MMQ lactotrophs and its accommodating role during slow firing and prolactin release

Authors :
Lecchi, M
Redaelli, E
Rosati, B
Gurrola, G
Florio, T
Crociani, O
Curia, G
Cassulini, R
Masi, A
Arcangeli, A
Olivotto, M
Schettini, G
Possani, L
Wanke, E
LECCHI, MARZIA MARIA
REDAELLI, ELISA
WANKE, ENZO
Lecchi, M
Redaelli, E
Rosati, B
Gurrola, G
Florio, T
Crociani, O
Curia, G
Cassulini, R
Masi, A
Arcangeli, A
Olivotto, M
Schettini, G
Possani, L
Wanke, E
LECCHI, MARZIA MARIA
REDAELLI, ELISA
WANKE, ENZO
Publication Year :
2002

Abstract

Native rat lactotrophs express thyrotrophin-releasing hormone-dependent K+ currents consisting of fast and slow deactivating components that are both sensitive to the class III anti-arrhythmic drugs that block the eag-related gene (ERG) K+ current (I(ERG)). Here we describe in MMQ prolactin-releasing pituitary cells the isolation of the slowly deactivating long-lasting component (I(ERGS)), which, unlike the fast component (I(ERGF)), is insensitive to verapamil 2 microm but sensitive to a novel scorpion toxin (ErgTx-2) that hardly affects I(ERGF). The time constants of I(ERGS) activation, deactivation, and recovery from inactivation are more than one order of magnitude greater than in I(ERGF), and the voltage-dependent inactivation is left-shifted by approximately 25 mV. The very slow MMQ firing frequency (approximately 0.2 Hz) investigated in perforated patch is increased approximately four times by anti-arrhythmic agents, by ErgTx-2, and by the abrupt I(ERGS) deactivation. Prolactin secretion in the presence of anti-arrhythmics is three- to fourfold higher in comparison with controls. We provide evidence from I(ERGS) and I(ERGF) simulations in a firing model cell to indicate that only I(ERGS) has an accommodating role during the experimentally observed very slow firing. Thus, we suggest that I(ERGS) potently modulates both firing and prolactin release in lactotroph cells

Details

Database :
OAIster
Notes :
English
Publication Type :
Electronic Resource
Accession number :
edsoai.on1308920328
Document Type :
Electronic Resource