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) All Versions of this Article: 555/2/331    most recent jphysiol.2003.054361v1 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 Hering, J. Articles by Lambert, R. C. Search for Related Content PubMed PubMed Citation Articles by Hering, J. Articles by Lambert, R. C.

Laboratoire de neurobiologie, Ecole Normale Supérieure, 46, rue d'Ulm, 75005 Paris, France

T-type calcium channels (the Ca_V3 channel family) are involved in defining the resting membrane potential and in neuronal activities such as oscillations and rebound depolarization. Their physiological roles depend upon the channel activation and inactivation kinetics. A fast inactivation that stops the ionic flux of calcium in tens of milliseconds has already been described in both native and heterologously expressed channels. Here, using HEK 293 cells expressing the rat Ca_V3.1 channel and whole-cell voltage clamp, we investigate an additional inactivation process, which can be distinguished from the previously described fast inactivation by its slow time course of recovery from inactivation (= 1 s) and by its sensitivity to external calcium. Steady-state slow inactivation is voltage dependent around the resting membrane potential (the potential of half-inactivation (V_0.5) =-70 mV, slope factor = 7.4 mV) and can reduce the calcium current by up to 50%. Near resting potential, the slow inactivation displays a half-time of induction of tens of seconds. The slow inactivation therefore modulates the availability of T-type calcium channels depending upon recent cell history, providing a mechanism to store information in a time scale of seconds.

(Received 12 September 2003; accepted after revision 12 December 2003; first published online 19 December 2003)
Corresponding author R. C. Lambert: Laboratoire de neurobiologie, Ecole Normale Supérieure, 46, rue d'Ulm, 75005 Paris, France. Email: rlambert{at}wotan.ens.fr

This article has been cited by other articles:

				M. A. Diana, Y. Otsu, G. Maton, T. Collin, M. Chat, and S. Dieudonne T-Type and L-Type Ca2+ Conductances Define and Encode the Bimodal Firing Pattern of Vestibulocerebellar Unipolar Brush Cells J. Neurosci., April 4, 2007; 27(14): 3823 - 3838. [Abstract] [Full Text] [PDF]

				B. S. Freeze, M. M. McNulty, and D. A. Hanck State-Dependent Verapamil Block of the Cloned Human Cav3.1 T-Type Ca2+ Channel Mol. Pharmacol., August 1, 2006; 70(2): 718 - 726. [Abstract] [Full Text] [PDF]

				M. Uebachs, C. Schaub, E. Perez-Reyes, and H. Beck T-type Ca2+ channels encode prior neuronal activity as modulated recovery rates J. Physiol., March 15, 2006; 571(3): 519 - 536. [Abstract] [Full Text] [PDF]

				N. Leresche, J. Hering, and R. C. Lambert Paradoxical Potentiation of Neuronal T-Type Ca2+ Current by ATP at Resting Membrane Potential J. Neurosci., June 16, 2004; 24(24): 5592 - 5602. [Abstract] [Full Text] [PDF]