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The Journal of Neuroscience, May 1, 2002, 22(9):3414-3425

Isolation of a Long-Lasting eag-Related Gene-Type K⁺ Current in MMQ Lactotrophs and Its Accommodating Role during Slow Firing and Prolactin Release

Marzia Lecchi¹, Elisa Redaelli¹, Barbara Rosati¹, Georgina Gurrola², Tullio Florio³, Olivia Crociani⁴, Giulia Curia¹, Rita Restano Cassulini¹, Alessio Masi⁴, Annarosa Arcangeli⁴, Massimo Olivotto⁴, Gennaro Schettini⁵, Lourival D. Possani², and Enzo Wanke¹

¹ Department of Biotechnology and Biosciences, University of Milano-Bicocca, I-20126 Milano, Italy, ² Department of Molecular Recognition and Structural Biology, Institute of Biotechnology, National Autonomous University of Mexico, Cuernavaca, Morelos 62271, Mexico, ³ Department of Biomedical Sciences, University G. D'Annunzio of Chieti, via dei Vestini, 66013 Chieti, Italy, ⁴ Department of General Pathology and Oncology, University of Firenze, I-50134 Firenze, Italy, and ⁵ Section of Pharmacology and Neurosciences, National Cancer Research Institute c/o Advanced Biotechnology Center, Department of Oncology, Biology, and Genetics, University of Genova, I-16132 Genova, Italy

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 µM 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 ~25 mV. The very slow MMQ firing frequency (~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.

Key words: K⁺ channels; lactotrophs; firing; anterior pituitary cells; erg genes; prolactin release

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Copyright © 2002 Society for Neuroscience  0270-6474/02/2293414-12$05.00/0

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