Modulation of L-type Ca2+ channel currents by various protein kinase activators and inhibitors in rat clonal pituitary GH3 cell line.
- Author:
Young Min BAE
1
;
Hye Jung BAEK
;
Ha Na CHO
;
Yung E EARM
;
Won Kyung HO
Author Information
1. Department of Physiology, Seoul National University College of Medicine, 28 Yeongeon-dong, Jongno-gu, Seoul, South Korea. wonkyung@snu.ac.kr
- Publication Type:Original Article
- Keywords:
GH3 cell;
L-type Ca2 channels;
Protein kinase
- MeSH:
Adenylyl Cyclases;
Animals;
Cell Line*;
Colforsin;
Cytosol;
Genistein;
Neuroendocrine Cells;
Nucleotides, Cyclic;
Patch-Clamp Techniques;
Phorbol 12,13-Dibutyrate;
Phosphotransferases;
Protein Kinase C;
Protein Kinases*;
Protein Tyrosine Phosphatases;
Protein-Tyrosine Kinases;
Rats*;
Vanadates
- From:The Korean Journal of Physiology and Pharmacology
2001;5(2):139-146
- CountryRepublic of Korea
- Language:English
-
Abstract:
L-type Ca2+ channels play an important role in regulating cytosolic Ca2+ and thereby regulating hormone secretions in neuroendocrine cells. Since hormone secretions are also regulated by various kinds of protein kinases, we investigated the role of some kinase activators and inhibitors in the regulation of the L-type Ca2+ channel currents in rat pituitary GH3 cells using the patch-clamp technique. Phorbol 12,13-dibutyrate (PDBu), a protein kinase C (PKC) activator, and vanadate, a protein tyrosine phosphatase (PTP) inhibitor, increased the Ba2+ current through the L-type Ca2+ channels. In contrast, bisindolylmaleimide I (BIM I), a PKC inhibitor, and genistein, a protein tyrosine kinase (PTK) inhibitor, suppressed the Ba2+ currents. Forskolin, an adenylate cyclase activator, and isobutyl methylxanthine (IBMX), a non-specific phosphodiesterase inhibitor, reduced Ba2+ currents. The above results show that the L-type Ca2+ channels are activated by PKC and PTK, and inhibited by elevation of cyclic nucleotides such as cAMP. From these results, it is suggested that the regulation of hormone secretion by various kinase activity in GH3 cells may be attributable, at least in part, to their effect on L-type Ca2+ channels.
