The ER is a central element in Ca2+ signaling, both as a modulator of cytoplasmic Ca2+ concentration ([Ca2+]i) and as a locus of Ca2+-regulated events. During surface membrane depolarization in excitable cells, the ER may either accumulate or release net Ca2+, but the conditions of stimulation that determine which form of net Ca2+ transport occurs are not well understood. The direction of net ER Ca2+ transport depends on the relative rates of Ca2+ uptake and release via distinct pathways that are differentially regulated by Ca2+, so we investigated these rates and their sensitivity to Ca2+ using sympathetic neurons as model cells. The rate of Ca2+ uptake by SERCAs (JSERCA), measured as the t-BuBHQ-sensitive component of the total cytoplasmic Ca2+ flux, increased monotonically with [Ca2+]i. Measurement of the rate of Ca2+ release (JRelease) during t-BuBHQ-induced [Ca2+]i transients made it possible to characterize the Ca2+ permeability of the ER (
Skip Nav Destination
Article navigation
1 March 2002
Article|
February 22 2002
Differential Regulation of ER Ca2+ Uptake and Release Rates Accounts for Multiple Modes of Ca2+-induced Ca2+ Release
Meredith A. Albrecht,
Meredith A. Albrecht
Department of Neurosciences, Case Western Reserve University, Cleveland, OH 44106
Search for other works by this author on:
Stephen L. Colegrove,
Stephen L. Colegrove
Department of Neurosciences, Case Western Reserve University, Cleveland, OH 44106
Search for other works by this author on:
David D. Friel
David D. Friel
Department of Neurosciences, Case Western Reserve University, Cleveland, OH 44106
Search for other works by this author on:
Meredith A. Albrecht
Department of Neurosciences, Case Western Reserve University, Cleveland, OH 44106
Stephen L. Colegrove
Department of Neurosciences, Case Western Reserve University, Cleveland, OH 44106
David D. Friel
Department of Neurosciences, Case Western Reserve University, Cleveland, OH 44106
Address correspondence to David Friel, Ph.D., Department of Neurosciences, Case Western Reserve University, 10900 Euclid Avenue, Cleveland, OH 44106. Fax: (216) 368-4650; E-mail: [email protected]
*
Abbreviations used in this paper: [Ca], total Ca concentration; FCCP, carbonyl cyanide p-(trifluoromethoxy)phenylhydrazone; InsP3R, d-myo-inositol 1,4,5-trisphosphate receptor; SERCA, sarco(endo)plasmic reticulum Ca ATPase; t-BuBHQ, 2,5-Di-(t-butyl)-1,4-hydroquinone; Tg, thapsigargin.
Received:
August 02 2001
Revision Received:
January 22 2002
Accepted:
January 25 2002
Online ISSN: 1540-7748
Print ISSN: 0022-1295
The Rockefeller University Press
2002
J Gen Physiol (2002) 119 (3): 211–233.
Article history
Received:
August 02 2001
Revision Received:
January 22 2002
Accepted:
January 25 2002
Connected Content
This article has been corrected
Correction
Citation
Meredith A. Albrecht, Stephen L. Colegrove, David D. Friel; Differential Regulation of ER Ca2+ Uptake and Release Rates Accounts for Multiple Modes of Ca2+-induced Ca2+ Release . J Gen Physiol 1 March 2002; 119 (3): 211–233. doi: https://doi.org/10.1085/jgp.20028484
Download citation file:
Sign in
Don't already have an account? Register
Client Account
You could not be signed in. Please check your email address / username and password and try again.
Could not validate captcha. Please try again.
Sign in via your Institution
Sign in via your InstitutionSuggested Content
The Voltage-sensitive Release Mechanism of Excitation Contraction Coupling in Rabbit Cardiac Muscle Is Explained by Calcium-induced Calcium Release
J Gen Physiol (April,2003)
Calcium-activated K+ Channels of Mouse β-cells are Controlled by Both Store and Cytoplasmic Ca2+ : Experimental and Theoretical Studies
J Gen Physiol (August,2002)
Allosteric Activation of Sodium–Calcium Exchange Activity by Calcium : Persistence at Low Calcium Concentrations
J Gen Physiol (October,2003)
Email alerts
Connected Content
Advertisement