The Journal of General Physiology
Axon Instruments microelectrode amplifiers
  Home | Help | Feedback | Subscriptions | Archive | Search | Table of Contents

This Article
Right arrow Full Text (PDF, 957K)
Right arrow Alert me when this article is cited
Right arrow Citation Map
Services
Right arrow Email this article
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new content in the JGP
Right arrow Download to citation manager
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via CrossRef
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Mlinar, B.
Right arrow Articles by Enyeart, J. J.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Mlinar, B.
Right arrow Articles by Enyeart, J. J.
Social Bookmarking
 Add to CiteULike   Add to Complore   Add to Connotea   Add to Del.icio.us   Add to Digg   Add to Reddit   Add to Technorati  
What's this?

The Journal of General Physiology, Vol 102, 239-255, Copyright © 1993 by The Rockefeller University Press


ARTICLES

Voltage-gated transient currents in bovine adrenal fasciculata cells. II. A-type K+ current

B Mlinar and JJ Enyeart
Department of Pharmacology, Ohio State University, Columbus 43210-1239.

In whole cell patch clamp recordings on enzymatically dissociated adrenal zona fasciculata (AZF) cells, a rapidly inactivating A-type K+ current was observed in each of more than 150 cells. Activation of IA was steeply voltage dependent and could be described by a Boltzmann function raised to an integer power of 4, with a midpoint of -28.3 mV. Using the "limiting logarithmic potential sensitivity," the single channel gating charge was estimated to be 7.2 e. Voltage-dependent inactivation could also be described by a Boltzmann function with a midpoint of -58.7 mV and a slope factor of 5.92 mV. Gating kinetics of IA included both voltage-dependent and -independent transitions in pathways between closed, open, and inactivated states. IA activated with voltage-dependent sigmoidal kinetics that could be fit with an n4h formalism. The activation time constant, tau a, reached a voltage- independent minimum at potentials positive to 0 mV. IA currents inactivated with two time constants that were voltage independent at potentials ranging from -30 to +45 mV. At +20 mV, tau i(fast) and tau i(slow) were 13.16 +/- 0.64 and 62.26 +/- 5.35 ms (n = 34), respectively. In some cells, IA inactivation kinetics slowed dramatically after many minutes of whole cell recording. Once activated by depolarization, IA channels returned to the closed state along pathways with two voltage-dependent time constants which were 0.208 s, tau rec-f and 10.02 s, tau rec-s at -80 mV. Approximately 90% of IA current recovered with slow kinetics at potentials between -60 and -100 mV. IA was blocked by 4-aminopyridine (IC50 = 629 microM) through a mechanism that was strongly promoted by channel activation. Divalent and trivalent cations including Ni2+ and La3+ also blocked IA with IC50's of 467 and 26.4 microM, respectively. With respect to biophysical properties and pharmacology, IA in AZF cells resembles to some extent transient K+ currents in neurons and muscle, where they function to regulate action potential frequency and duration. The function of this prominent current in steroid hormone secretion by endocrine cells that may not generate action potentials is not yet clear.
Add to CiteULike CiteULike   Add to Complore Complore   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us   Add to Digg Digg   Add to Reddit Reddit   Add to Technorati Technorati    What's this?


This article has been cited by other articles:


Home page
JGPHome page
H. Liu, J. A. Enyeart, and J. J. Enyeart
ACTH Inhibits bTREK-1 K+ Channels through Multiple cAMP-dependent Signaling Pathways
J. Gen. Physiol., August 1, 2008; 132(2): 279 - 294.
[Abstract] [Full Text] [PDF]


Home page
J. Pharmacol. Exp. Ther.Home page
H. Liu, J. A. Enyeart, and J. J. Enyeart
Potent Inhibition of Native TREK-1 K+ Channels by Selected Dihydropyridine Ca2+ Channel Antagonists
J. Pharmacol. Exp. Ther., October 1, 2007; 323(1): 39 - 48.
[Abstract] [Full Text] [PDF]


Home page
Am. J. Physiol. Cell Physiol.Home page
H. Liu, J. A. Enyeart, and J. J. Enyeart
Angiotensin II inhibits native bTREK-1 K+ channels through a PLC-, kinase C-, and PIP2-independent pathway requiring ATP hydrolysis
Am J Physiol Cell Physiol, August 1, 2007; 293(2): C682 - C695.
[Abstract] [Full Text] [PDF]


Home page
J. Biol. Chem.Home page
J. J. Enyeart, S. J. Danthi, H. Liu, and J. A. Enyeart
Angiotensin II Inhibits bTREK-1 K+ Channels in Adrenocortical Cells by Separate Ca2+- and ATP Hydrolysis-dependent Mechanisms
J. Biol. Chem., September 2, 2005; 280(35): 30814 - 30828.
[Abstract] [Full Text] [PDF]


Home page
Am. J. Physiol. Endocrinol. Metab.Home page
J. A. Enyeart, S. J. Danthi, and J. J. Enyeart
TREK-1 K+ channels couple angiotensin II receptors to membrane depolarization and aldosterone secretion in bovine adrenal glomerulosa cells
Am J Physiol Endocrinol Metab, December 1, 2004; 287(6): E1154 - E1165.
[Abstract] [Full Text] [PDF]


Home page
Mol. Pharmacol.Home page
J. A. Enyeart, S. Danthi, and J. J. Enyeart
Corticotropin Induces the Expression of TREK-1 mRNA and K+ Current in Adrenocortical Cells
Mol. Pharmacol., July 1, 2003; 64(1): 132 - 142.
[Abstract] [Full Text] [PDF]


Home page
J. Biol. Chem.Home page
J. J. Enyeart, L. Xu, S. Danthi, and J. A. Enyeart
An ACTH- and ATP-regulated Background K+ Channel in Adrenocortical Cells Is TREK-1
J. Biol. Chem., December 13, 2002; 277(51): 49186 - 49199.
[Abstract] [Full Text] [PDF]


Home page
Am. J. Physiol. Endocrinol. Metab.Home page
J. J. Enyeart, L. Xu, and J. A. Enyeart
Dual actions of lanthanides on ACTH-inhibited leak K+ channels
Am J Physiol Endocrinol Metab, June 1, 2002; 282(6): E1255 - E1266.
[Abstract] [Full Text] [PDF]


Home page
J. Pharmacol. Exp. Ther.Home page
L. Xu, J. A. Enyeart, and J. J. Enyeart
Neuroprotective Agent Riluzole Dramatically Slows Inactivation of Kv1.4 Potassium Channels by a Voltage-Dependent Oxidative Mechanism
J. Pharmacol. Exp. Ther., October 1, 2001; 299(1): 227 - 237.
[Abstract] [Full Text] [PDF]


Home page
Mol. Pharmacol.Home page
J. J. Enyeart, L. Xu, J. C. Gomora, and J. A. Enyeart
Reciprocal Modulation of Voltage-Gated and Background K+ Channels Mediated by Nucleotides and Corticotropin
Mol. Pharmacol., July 1, 2001; 60(1): 114 - 123.
[Abstract] [Full Text]


Home page
Am. J. Physiol. Cell Physiol.Home page
L. Xu and J. J. Enyeart
Properties of ATP-dependent K+ channels in adrenocortical cells
Am J Physiol Cell Physiol, January 1, 2001; 280(1): C199 - C215.
[Abstract] [Full Text] [PDF]


Home page
J. Pharmacol. Exp. Ther.Home page
J. C. Gomora, L. Xu, J. A. Enyeart, and J. J. Enyeart
Effect of Mibefradil on Voltage-Dependent Gating and Kinetics of T-Type Ca2+ Channels in Cortisol-Secreting Cells
J. Pharmacol. Exp. Ther., January 1, 2000; 292(1): 96 - 103.
[Abstract] [Full Text]


Home page
Mol. Pharmacol.Home page
J. C. Gomora, J. A. Enyeart, and J. J. Enyeart
Mibefradil Potently Blocks ATP-Activated K+ Channels in Adrenal Cells
Mol. Pharmacol., December 1, 1999; 56(6): 1192 - 1197.
[Abstract] [Full Text]


Home page
J. Pharmacol. Exp. Ther.Home page
J. C. Gomora and J. J. Enyeart
Dual Pharmacological Properties of a Cyclic AMP-Sensitive Potassium Channel
J. Pharmacol. Exp. Ther., July 1, 1999; 290(1): 266 - 275.
[Abstract] [Full Text]


Home page
J. Pharmacol. Exp. Ther.Home page
O. Soriani, F. L. Foll, F. Roman, F. P. Monnet, H. Vaudry, and L. Cazin
A-Current Down-Modulated by sigma  Receptor in Frog Pituitary Melanotrope Cells Through a G Protein-Dependent Pathway
J. Pharmacol. Exp. Ther., April 1, 1999; 289(1): 321 - 328.
[Abstract] [Full Text]


Home page
Mol. Pharmacol.Home page
L. Xu and J. J. Enyeart
Purine and Pyrimidine Nucleotides Inhibit a Noninactivating K+ Current and Depolarize Adrenal Cortical Cells through a G Protein-Coupled Receptor
Mol. Pharmacol., February 1, 1999; 55(2): 364 - 376.
[Abstract] [Full Text]


Home page
Am. J. Physiol. Cell Physiol.Home page
J. C. Gomora and J. J. Enyeart
Ca2+ depolarizes adrenal cortical cells through selective inhibition of an ATP-activated K+ current
Am J Physiol Cell Physiol, December 1, 1998; 275(6): C1526 - C1537.
[Abstract] [Full Text] [PDF]


Home page
J. Biol. Chem.Home page
B. Mlinar, B. A. Biagi, and J. J. Enyeart
Losartan-sensitive AII Receptors Linked to Depolarization- dependent Cortisol Secretion through a Novel Signaling Pathway
J. Biol. Chem., September 8, 1995; 270(36): 20942 - 20951.
[Abstract] [Full Text] [PDF]


Home page
J. Biol. Chem.Home page
J. A. Enyeart, L. Xu, and J. J. Enyeart
A Bovine Adrenocortical Kv1.4 K+ Channel Whose Expression Is Potently Inhibited by ACTH
J. Biol. Chem., October 27, 2000; 275(44): 34640 - 34649.
[Abstract] [Full Text] [PDF]



  Home | Help | Feedback | Subscriptions | Archive | Search | Table of Contents