This Article Full Text Full Text (PDF) Purchase Article View Shopping Cart Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Copyright Permission Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Kato, M. Articles by Sakuma, Y. Search for Related Content PubMed PubMed Citation Articles by Kato, M. Articles by Sakuma, Y.

Regulation by Growth Hormone-Releasing Hormone and Somatostatin of a Na⁺ Current in the Primary Cultured Rat Somatotroph¹

Department of Physiology I, Nippon Medical School, Sendagi 1, Bunkyo Tokyo 113, Japan

Address all correspondence and requests for reprints to: M. Kato, Department of Physiology I, Nippon Medical School, Sendagi 1, Bunkyo Tokyo 113, Japan. E-mail: mkato{at}nms.ac.jp

The purpose of the present study is to characterize Na⁺ current activated by GH-releasing hormone (GHRH) and to investigate the effect of somatostatin (SRIF) on that current, because the Na⁺ current has been suggested to play a pivotal role in the process of GHRH-induced GH secretion. Primary-cultured pituitary somatotrophs were prepared from male Wistar rats. Whole-cell membrane currents were recorded and analyzed by a perforated patch clamp system. To isolate Na⁺ current, K⁺ and Ca²⁺ were replaced with Cs⁺ and Mg²⁺, respectively, in the extracellular solution, and cesium aspartate was used for the pipette solution. Furthermore, tetrodotoxin and nifedipine were added to the extracellular solution to eliminate the voltage-gated currents. Under these conditions, GHRH activated a mean inward Na⁺ current (-1.86 ± 0.33 pA, mean ± SE) at potentials between -50 and -20 mV and a smaller current (-0.59 ± 0.13 pA) at potentials between -100 and -80 mV, which were completely blocked by protein kinase A blocker (H-89). In addition, SRIF (1-10 nM) partially suppressed these Na⁺ currents, which were not affected by phosphatase inhibitors (okadaic acid and calyculin A). These results suggest that GHRH activates the Na⁺ current through phosphorylation by protein kinase A and that SRIF partially suppressed this current and that the current was larger at more positive potentials than at more negative potentials.

This article has been cited by other articles:

				K. Tsaneva-Atanasova, A. Sherman, F. van Goor, and S. S. Stojilkovic Mechanism of Spontaneous and Receptor-Controlled Electrical Activity in Pituitary Somatotrophs: Experiments and Theory J Neurophysiol, July 1, 2007; 98(1): 131 - 144. [Abstract] [Full Text] [PDF]

				Y. Miura and H. Matsui Glucagon-like peptide-1 induces a cAMP-dependent increase of [Na+]i associated with insulin secretion in pancreatic {beta}-cells Am J Physiol Endocrinol Metab, November 1, 2003; 285(5): E1001 - E1009. [Abstract] [Full Text] [PDF]

				K. Kaneishi, Y. Sakuma, H. Kobayashi, and M. Kato 3',5'-Cyclic Adenosine Monophosphate Augments Intracellular Ca2+ Concentration and Gonadotropin-Releasing Hormone (GnRH) Release in Immortalized GnRH Neurons in an Na+-Dependent Manner Endocrinology, November 1, 2002; 143(11): 4210 - 4217. [Abstract] [Full Text] [PDF]

				J. L. Ramírez, J. P. Castaño, R. Torronteras, A. J. Martínez-Fuentes, L. S. Frawley, S. García-Navarro, and F. Gracia-Navarro Growth Hormone (GH)-Releasing Factor Differentially Activates Cyclic Adenosine 3',5'-Monophosphate- and Inositol Phosphate-Dependent Pathways to Stimulate GH Release in Two Porcine Somatotrope Subpopulations Endocrinology, April 1, 1999; 140(4): 1752 - 1759. [Abstract] [Full Text]

				R. I. Fonteriz, C. Villalobos, and J. Garcia-Sancho An extracellular sulfhydryl group modulates background Na+ conductance and cytosolic Ca2+ in pituitary cells Am J Physiol Cell Physiol, April 1, 2002; 282(4): C864 - C872. [Abstract] [Full Text] [PDF]