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

This Article Full Text 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 Martínez-Pinna, J. Articles by Gallego, R. Search for Related Content PubMed PubMed Citation Articles by Martínez-Pinna, J. Articles by Gallego, R.

Distinct mechanisms for activation of Cl^- and K⁺ currents by Ca²⁺ from different sources in mouse sympathetic neurones

Juan Martínez-Pinna, Elspeth M. McLachlan* and Roberto Gallego

1. We have investigated the roles of different voltage-dependent Ca²⁺ channels in the activation of the Cl^- and K⁺ channels responsible for the afterdepolarization (ADP) and slow afterhyperpolarization (AHP) in sympathetic neurones of the isolated mouse superior cervical ganglion in vitro.

2. The ADP and its associated Ca²⁺-activated Cl^- current were markedly decreased by -agatoxin IVA (40-200 nM) and nifedipine (1-10 µM), but not by -conotoxin GVIA (300 nM).

3. In contrast, the AHP and the apamin-sensitive Ca²⁺-activated K⁺ current that underlies this potential were blocked by -conotoxin GVIA, but were not affected by -agatoxin IVA and were only slightly reduced by nifedipine.

4. Ryanodine (20 µM) reduced the Ca²⁺-activated Cl^- current following an action potential by 75 % but on average did not affect the Ca²⁺-activated K⁺ current.

5. Evidence that R-type channels provide a proportion of the Ca²⁺ activating both types of Ca²⁺-dependent channel was obtained.

6. We conclude that Ca²⁺ entering through L- and P-type Ca²⁺ channels preferentially activates the Cl^- current responsible for the ADP in mouse sympathetic neurones, predominantly via Ca²⁺-induced Ca²⁺ release, whereas the Ca²⁺ that activates the K⁺ channels responsible for the AHP enters predominantly through N-type channels. The data can be explained by the selective association of each type of Ca²⁺ channel with particular intracellular mechanisms for activating other membrane channels, one indirect and the other direct, probably located at discrete sites on the soma and dendrites.

This article has been cited by other articles:

				D. Wicher, J. Berlau, C. Walther, and A. Borst Peptidergic Counter-Regulation of Ca2+- and Na+-Dependent K+ Currents Modulates the Shape of Action Potentials in Neurosecretory Insect Neurons J Neurophysiol, January 1, 2006; 95(1): 311 - 322. [Abstract] [Full Text] [PDF]

				X. Gasull, X. Liao, M. F. Dulin, C. Phelps, and E. T. Walters Evidence That Long-Term Hyperexcitability of the Sensory Neuron Soma Induced by Nerve Injury in Aplysia Is Adaptive J Neurophysiol, September 1, 2005; 94(3): 2218 - 2230. [Abstract] [Full Text] [PDF]

				A. Verkhratsky Physiology and Pathophysiology of the Calcium Store in the Endoplasmic Reticulum of Neurons Physiol Rev, January 1, 2005; 85(1): 201 - 279. [Abstract] [Full Text] [PDF]

				R. K. Cloues and W. A. Sather Afterhyperpolarization Regulates Firing Rate in Neurons of the Suprachiasmatic Nucleus J. Neurosci., March 1, 2003; 23(5): 1593 - 1604. [Abstract] [Full Text] [PDF]

				E. Lancaster, E. J. Oh, T. Gover, and D. Weinreich Calcium and calcium-activated currents in vagotomized rat primary vagal afferent neurons J. Physiol., April 15, 2002; 540(2): 543 - 556. [Abstract] [Full Text] [PDF]