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This Article Full Text Full Text (PDF) Supplemental Data All Versions of this Article: 571/3/519    most recent jphysiol.2005.103614v1 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 Uebachs, M. Articles by Beck, H. Search for Related Content PubMed PubMed Citation Articles by Uebachs, M. Articles by Beck, H. Related Collections Molecular and Genomic Related Article

¹ Department of Epileptology, University of Bonn Medical Center, Sigmund-Freud-Strasse 25, 53105 Bonn, Germany
² Department of Pharmacology, University of Virginia, Charlottesville, VA 22908, USA

T-type Ca²⁺ channels give rise to low-threshold inward currents that are central determinants of neuronal excitability. The availability of T-type Ca²⁺ channels is strongly influenced by voltage-dependent inactivation and recovery from inactivation. Here, we show that native and cloned T-type Ca²⁺ channel subunits selectively encode specific aspects of prior membrane potential changes via a powerful modulation of the rates with which these channels recover from inactivation. Increasing the duration of subthreshold (–70 to –55 mV) conditioning depolarizations caused a pronounced slowing of subsequent recovery from inactivation of both cloned (Ca_v3.1–3.3) and native T-type channels (thalamic neurones). The scaling of recovery rates with increasing duration of conditioning depolarizations could be well described by a power law function. Different T-type channel isoforms exhibited overlapping but complementary ranges of recovery rates. Intriguingly, scaling of recovery rates was dramatically reduced in Ca_v3.2 and Ca_v3.3, but not Ca_v3.1 subunits, when mock action potentials were superimposed on conditioning depolarizations. Our results suggest that different T-type channel subunits exhibit dramatic differences in scaling relationships, in addition to well-described differences in other biophysical properties. Furthermore, the availability of T-type channels is powerfully modulated over time, depending on the patterns of prior activity that these channels have encountered. These data provide a novel mechanism for cellular short-term plasticity on the millisecond to second time scale that relies on biophysical properties of specific T-type Ca²⁺ channel subunits.

(Received 15 December 2005; accepted after revision 12 January 2006; first published online 19 January 2006)
Corresponding author H. Beck: Laboratory of Experimental Epileptology, Department of Epileptology, University of Bonn, Sigmund-Freud-Strasse 25, D-53105 Bonn, Germany. Email: heinz.beck{at}ukb.uni-bonn.de

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