HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text (PDF) 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 Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Herrington, J Articles by Lingle, C J Search for Related Content PubMed PubMed Citation Articles by Herrington, J Articles by Lingle, C J

Department of Anesthesiology, Washington University School of Medicine, St Louis, MO 63110, USA.

1. The mechanism by which muscarine, ionomycin or caffeine results in suppression of Ca(2+)- and voltage-dependent outward current in rat adrenal chromaffin cells was evaluated using both whole-cell voltage clamp and single channel recording. 2. The whole-cell current activated following the elevation of the cytosolic calcium concentration ([Ca2+]i) by muscarine inactivates with a time course comparable to that of single Ca(2+)- and voltage-dependent potassium (BK) channels. 3. The whole-cell inactivating current is pharmacologically similar to BK current. 4. The voltage dependence of inactivation and rate of recovery from inactivation are qualitatively similar for both whole-cell current and ensemble averages of single BK channels. Furthermore, changes in the rate of whole-cell current inactivation track expected changes in submembrane [Ca2+]. 5. The suppression of outward current can be accounted for solely by inactivation of BK channels and does not depend on the means by which [Ca2+]i is elevated. 6. Muscarinic acetylcholine receptor (mAChR) activation, changes in holding potential (-50 to -20 mV), and step depolarizations of different amplitude and duration were tested for their ability to elevate [Ca2+]i and thereby regulate the availability of BK current for activation. 7. Following muscarine-induced elevation of [Ca2+]i at holding potentials positive to -40 mV, the availability of BK current for activation was typically reduced by more than 50%. 8. Holding potentials in the range of -50 to -20 mV produced only slight alterations in the availability of BK current for activation. 9. Step depolarizations that cause maximal rates of Ca2+ influx (0 to +10 mV) must exceed 200 ms to reduce the availability of BK current by approximately 50%. 10. The results show that the muscarine-induced elevation of [Ca2+]i produces a profound reduction in the availability of BK channels for activation at membrane potentials likely to be physiologically meaningful. Although depolarization- induced Ca2+ influx can inactivate BK current, we propose that short duration depolarizations that occur during normal electrical activity will not significantly alter BK channel availability.

This article has been cited by other articles:

				X. Zhang, X. Zeng, and C. J. Lingle Slo3 K+ Channels: Voltage and pH Dependence of Macroscopic Currents J. Gen. Physiol., August 28, 2006; 128(3): 317 - 336. [Abstract] [Full Text] [PDF]

				X.-H. Zeng, X.-M. Xia, and C. J. Lingle Divalent Cation Sensitivity of BK Channel Activation Supports the Existence of Three Distinct Binding Sites J. Gen. Physiol., February 28, 2005; 125(3): 273 - 286. [Abstract] [Full Text] [PDF]

				K. Duan, X. Yu, C. Zhang, and Z. Zhou Control of Secretion by Temporal Patterns of Action Potentials in Adrenal Chromaffin Cells J. Neurosci., December 3, 2003; 23(35): 11235 - 11243. [Abstract] [Full Text] [PDF]

				P. V. Lovell and D. P. McCobb Pituitary Control of BK Potassium Channel Function and Intrinsic Firing Properties of Adrenal Chromaffin Cells J. Neurosci., May 15, 2001; 21(10): 3429 - 3442. [Abstract] [Full Text] [PDF]

				P. V. Lovell, D. G. James, and D. P. McCobb Bovine Versus Rat Adrenal Chromaffin Cells: Big Differences in BK Potassium Channel Properties J Neurophysiol, June 1, 2000; 83(6): 3277 - 3286. [Abstract] [Full Text] [PDF]

				M. Prakriya and C. J. Lingle BK Channel Activation by Brief Depolarizations Requires Ca2+ Influx Through L- and Q-Type Ca2+ Channels in Rat Chromaffin Cells J Neurophysiol, May 1, 1999; 81(5): 2267 - 2278. [Abstract] [Full Text] [PDF]

				Z.-W. Li, J. P. Ding, V. Kalyanaraman, and C. J. Lingle RINm5f Cells Express Inactivating BK Channels Whereas HIT Cells Express Noninactivating BK Channels J Neurophysiol, February 1, 1999; 81(2): 611 - 624. [Abstract] [Full Text] [PDF]

				Z.-M. Pei, V. M. Baizabal-Aguirre, G. J. Allen, and J. I. Schroeder A transient outward-rectifying K+ channel current down-regulated by cytosolic Ca2+ in Arabidopsis thaliana guard cells PNAS, May 26, 1998; 95(11): 6548 - 6553. [Abstract] [Full Text] [PDF]

				M. Saito, C. Nelson, L. Salkoff, and C. J. Lingle A Cysteine-rich Domain Defined by a Novel Exon in a Slo Variant in Rat Adrenal Chromaffin Cells and PC12 Cells J. Biol. Chem., May 2, 1997; 272(18): 11710 - 11717. [Abstract] [Full Text] [PDF]

				M. Prakriya, C. R. Solaro, and C. J. Lingle [Ca2+]i Elevations Detected by BK Channels during Ca2+ Influx and Muscarine-Mediated Release of Ca2+ from Intracellular Stores in Rat Chromaffin Cells J. Neurosci., July 15, 1996; 16(14): 4344 - 4359. [Abstract] [Full Text] [PDF]