|
||
The Journal of General Physiology, Vol 104, 1019-1038, Copyright © 1994 by The Rockefeller University Press
ARTICLES |
U Meza, G Avila, R Felix, JC Gomora and G Cota
Department of Physiology, Biophysics, and Neurosciences, National Polytechnic Institute, Mexico, D.F., Mexico.
In rat pituitary GH3 cells, epidermal growth factor (EGF) and insulin stimulate prolactin production, whereas glucocorticoids exert the opposite effect. In the present study, GH3 cells were subjected to whole-cell patch clamp to assess the chronic actions of such regulatory factors on voltage-dependent calcium currents. Before the electrical recording, cells were grown 5-6 d either under standard conditions or in the presence of 5 nM EGF, 100 nM insulin, 1 microM dexamethasone or 5 microM cortisol. EGF induced a twofold selective increase in high- threshold calcium current density. Insulin and glucocorticoids, on the other hand, specifically regulated low-threshold Ca channels. Current density through these channels increased by 70% in insulin-treated cells, and decreased by 50% in cells exposed to dexamethasone or cortisol. Other Ca channel properties investigated (conductance-voltage curves, deactivation rates, time course and voltage dependence of low- threshold current inactivation) were unaffected by the chemical messengers. The alterations in current density persisted for many hours after removing the regulatory factors from the culture medium. In fact, the stimulatory action of EGF on high-threshold current lasted > 3 d. The results suggest that the control of prolactin production by the factors tested involves regulation of the surface density of functional Ca channels in the plasma membrane.
This article has been cited by other articles:
![]() |
S.-K. Yang, H. C. Parkington, J. Epelbaum, D. J. Keating, and C. Chen Somatostatin decreases voltage-gated Ca2+ currents in GH3 cells through activation of somatostatin receptor 2 Am J Physiol Endocrinol Metab, June 1, 2007; 292(6): E1863 - E1870. [Abstract] [Full Text] [PDF] |
||||
![]() |
L. F. Lopez-Santiago, M. Pertin, X. Morisod, C. Chen, S. Hong, J. Wiley, I. Decosterd, and L. L. Isom Sodium channel beta2 subunits regulate tetrodotoxin-sensitive sodium channels in small dorsal root ganglion neurons and modulate the response to pain. J. Neurosci., July 26, 2006; 26(30): 7984 - 7994. [Abstract] [Full Text] [PDF] |
||||
![]() |
A. M. Lopez-Dominguez, J. L. Espinosa, A. Navarrete, G. Avila, and G. Cota Nerve growth factor affects Ca2+ currents via the p75 receptor to enhance prolactin mRNA levels in GH3 rat pituitary cells J. Physiol., July 15, 2006; 574(2): 349 - 365. [Abstract] [Full Text] [PDF] |
||||
![]() |
E. Zebedin, W. Sandtner, S. Galler, J. Szendroedi, H. Just, H. Todt, and K. Hilber Fiber type conversion alters inactivation of voltage-dependent sodium currents in murine C2C12 skeletal muscle cells Am J Physiol Cell Physiol, August 1, 2004; 287(2): C270 - C280. [Abstract] [Full Text] [PDF] |
||||
![]() |
O. Delbono, M. Renganathan, and M. L. Messi Regulation of Mouse Skeletal Muscle L-Type Ca2+ Channel by Activation of the Insulin-Like Growth Factor-1 Receptor J. Neurosci., September 15, 1997; 17(18): 6918 - 6928. [Abstract] [Full Text] [PDF] |
||||
|
|