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T‐type Ca 2+ channels encode prior neuronal activity as modulated recovery rates
Author(s) -
Uebachs M.,
Schaub C.,
PerezReyes E.,
Beck H.
Publication year - 2006
Publication title -
the journal of physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.802
H-Index - 240
eISSN - 1469-7793
pISSN - 0022-3751
DOI - 10.1113/jphysiol.2005.103614
Subject(s) - encode , neuroscience , premovement neuronal activity , chemistry , biology , genetics , gene
T‐type Ca 2+ channels give rise to low‐threshold inward currents that are central determinants of neuronal excitability. The availability of T‐type Ca 2+ channels is strongly influenced by voltage‐dependent inactivation and recovery from inactivation. Here, we show that native and cloned T‐type Ca 2+ 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 v 3.1–3.3) 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 v 3.2 and Ca v 3.3, but not Ca v 3.1 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 Ca 2+ channel subunits.