The Journal of General Physiology
  Home | Help | Feedback | Subscriptions | Archive | Search | Table of Contents
This Article
Right arrow Full Text
Right arrow Full Text (PDF, 320K)
Right arrow PPT slides of all figures
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 Harkins, A. B.
Right arrow Articles by Fox, A. P.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Harkins, A. B.
Right arrow Articles by Fox, A. P.
Social Bookmarking
Add to CiteULike   Add to Complore   Add to Connotea   Add to Del.icio.us   Add to Digg   Add to Facebook   Add to Reddit   Add to Technorati   Add to Twitter  
What's this?
© The Rockefeller University Press, 0022-1295/1998//257/ $5.00
Journal of General Physiology, Volume 111, Number 2, 1998

Article

Activation of Nicotinic Acetylcholine Receptors Augments Calcium Channel-mediated Exocytosis in Rat Pheochromocytoma (PC12) Cells

Amy B. Harkins and Aaron P. Fox

From the Department of Pharmacological and Physiological Sciences, The University of Chicago, Chicago, Illinois 60637

The functional effect of activating Ca2+-permeable neuronal nicotinic acetylcholine receptors (nAChRs) on vesicle secretion was studied in PC12 cells. Single cells were patch-clamped in the whole-cell configuration and stimulated with either brief pulses of nicotine to activate the Ca2+-permeable nAChRs or with voltage steps to activate voltage-dependent Ca2+ channels. Membrane capacitance was used as a measure of vesicle secretion. Activation of nAChRs by nicotine application to cells voltage clamped at –80 mV evoked secretion. This secretion was completely abolished by nicotinic antagonists. When the cells were voltage clamped at +20 mV in the presence of Cd2+ to block voltage-activated Ca2+ channels, nicotine elicited a small amount of secretion. Most interestingly, when the nAChRs were activated coincidentally with voltage-dependent Ca2+ channels, secretion was augmented approximately twofold over the secretion elicited with voltage-dependent Ca2+ channels alone. Our data suggest that Ca2+ influx via nAChRs affects Ca2+-dependent cellular functions, including vesicle secretion. In addition to the secretion evoked by nAChR activation at hyperpolarized potentials, we demonstrate that even at depolarized potentials, nAChRs provide an important Ca2+ entry pathway underlying Ca2+-dependent cellular processes such as exocytosis.

Key Words: acetylcholine receptor • exocytosis • Ca2+ channels • nicotine • secretion

Address correspondence to Amy B. Harkins, The Department of Pharmacological and Physiological Sciences, The University of Chicago, 947 E. 58th Street, Chicago, IL 60637. Fax: 773-702-1216; E-mail: amy{at}drugs.bsd.uchicago.edu or aaron{at}drugs.bsd.uchicago.edu


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 Facebook Facebook   Add to Reddit Reddit   Add to Technorati Technorati   Add to Twitter Twitter    What's this?


This article has been cited by other articles:


Home page
 Am. J. Physiol. Cell Physiol.Home page
L. Tapia, J. Garcia-Eguiagaray, A. G. Garcia, and L. Gandia
Preconditioning stimuli that augment chromaffin cell secretion
Am J Physiol Cell Physiol, April 1, 2009; 296(4): C792 - C800.
[Abstract] [Full Text] [PDF]

Home page
 Proc. Natl. Acad. Sci. USAHome page
A. B. Harkins, A. L. Cahill, J. F. Powers, A. S. Tischler, and A. P. Fox
Deletion of the synaptic protein interaction site of the N-type (CaV2.2) calcium channel inhibits secretion in mouse pheochromocytoma cells
PNAS, October 19, 2004; 101(42): 15219 - 15224.
[Abstract] [Full Text] [PDF]

Home page
 J. Neurophysiol.Home page
A. B. Harkins, A. L. Cahill, J. F. Powers, A. S. Tischler, and A. P. Fox
Expression of Recombinant Calcium Channels Support Secretion in a Mouse Pheochromocytoma Cell Line
J Neurophysiol, October 1, 2003; 90(4): 2325 - 2333.
[Abstract] [Full Text] [PDF]

Home page
 J. Neurosci.Home page
N. Bernardini, S. K. Sauer, R. Haberberger, M. J. M. Fischer, and P. W. Reeh
Excitatory Nicotinic and Desensitizing Muscarinic (M2) Effects on C-Nociceptors in Isolated Rat Skin
J. Neurosci., May 1, 2001; 21(9): 3295 - 3302.
[Abstract] [Full Text] [PDF]

Home page
 J. Immunol.Home page
N. G. Carlson, W. A. Wieggel, J. Chen, A. Bacchi, S. W. Rogers, and L. C. Gahring
Inflammatory Cytokines IL-1{alpha}, IL-1{beta}, IL-6, and TNF-{alpha} Impart Neuroprotection to an Excitotoxin Through Distinct Pathways
J. Immunol., October 1, 1999; 163(7): 3963 - 3968.
[Abstract] [Full Text] [PDF]

Home page
 Proc. Natl. Acad. Sci. USAHome page
Y.-J. Cao and Y.-Y. Peng
Activation of nicotinic receptor-induced postsynaptic responses to luteinizing hormone-releasing hormone in bullfrog sympathetic ganglia via a Na+-dependent mechanism
PNAS, October 13, 1998; 95(21): 12689 - 12694.
[Abstract] [Full Text] [PDF]


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