%0 Journal Article
%T Potassium Current Is Not Affected by Long-Term Exposure to Ghrelin or GHRP-6 in Somatotropes GC Cells
%A Belisario Dom¨ªnguez Mancera
%A Eduardo Monjaraz Guzman
%A Jorge L. V. Flores-Hern¨¢ndez
%A Manuel Barrientos Morales
%A Jos¨¦ M. Mart¨ªnez Hernandez
%A Antonio Hern¨¢ndez Beltran
%A Patricia Cervantes Acosta
%J Journal of Biophysics
%D 2013
%I Hindawi Publishing Corporation
%R 10.1155/2013/913792
%X Ghrelin is a growth hormone (GH) secretagogue (GHS) and GHRP-6 is a synthetic peptide analogue; both act through the GHS receptor. GH secretion depends directly on the intracellular concentration of Ca2+; this is determined from the intracellular reserves and by the entrance of Ca2+ through the voltage-dependent calcium channels, which are activated by the membrane depolarization. Membrane potential is mainly determined by K+ channels. In the present work, we investigated the effect of ghrelin (10£¿nM) or GHRP-6 (100£¿nM) for 96£¿h on functional expression of voltage-dependent K+ channels in rat somatotropes: GC cell line. Physiological patch-clamp whole-cell recording was used to register the K+ currents. With Cd2+ (1£¿mM) and tetrodotoxin (1£¿¦Ìm) in the bath solution recording, three types of currents were characterized on the basis of their biophysical and pharmacological properties. GC cells showed a K+ current with a transitory component sensitive to 4-aminopyridine, which represents ~40% of the total outgoing current; a sustained component named delayed rectifier , sensitive to tetraethylammonium; and a third type of K+ current was recorded at potentials more negative than £¿80£¿mV, permitting the entrance of K+ named inward rectifier (KIR). Chronic treatment with ghrelin or GHRP-6 did not modify the functional expression of K+ channels, without significant changes ( ) in the amplitudes of the three currents observed; in addition, there were no modifications in their biophysical properties and kinetic activation or inactivation. 1. Introduction The growth hormone is mainly under the control of two hypothalamic neuropeptides acting in opposition: one, the growth hormone releasing hormone (GHRH), as a stimulant, and the other, somatostatin, as an inhibitor [1, 2]. The GHRH specifically bind to its receptor on the plasmatic membrane of the somatotropes; this increments the activity of adenylate cyclase, which increases the generation of AMPc [3, 4]. This increase in the AMPc levels let to open the voltage-dependent Ca2+ channels [5, 6] and a rapid increase in the intracellular Ca2+ concentration [Ca2+], thus promoting the exocytosis of GH [7, 8]. The inhibitory effect of somatostatin involves the inhibition of adenylate cyclase activity and a reduction of [9, 10]. In addition to the GHRH, a group of synthetic oligopeptides releasing GH (GHRPs) or GH secretagogues (GHS) are capable of stimulating the secretion of GH [2, 11, 12]. The GH-releasing peptide-6 (GHRP-6) is one of the most representative of those compounds [2, 11¨C13]. Research on the mechanism of
%U http://www.hindawi.com/journals/jbp/2013/913792/