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Distinct kinetics of cloned T‐type Ca 2 + channels lead to differential Ca 2 + entry and frequency‐dependence during mock action potentials
Author(s) -
Kozlov Andrei S.,
McKenna Frank,
Lee JungHa,
Cribbs Leanne L.,
PerezReyes Edward,
Feltz Anne,
Lambert Régis C.
Publication year - 1999
Publication title -
european journal of neuroscience
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.346
H-Index - 206
eISSN - 1460-9568
pISSN - 0953-816X
DOI - 10.1046/j.1460-9568.1999.00841.x
Subject(s) - biophysics , chemistry , membrane potential , kinetics , electrophysiology , stimulation , patch clamp , voltage dependent calcium channel , ion channel , physics , neuroscience , calcium , biochemistry , biology , receptor , quantum mechanics , organic chemistry
Voltage‐dependent activity around the resting potential is determinant in neuronal physiology and participates in the definition of the firing pattern. Low‐voltage‐activated T‐type Ca 2 + channels directly affect the membrane potential and control a number of secondary Ca 2 + ‐dependent permeabilities. We have studied the ability of the cloned T‐type channels (α1G,H,I) to carry Ca 2 + currents in response to mock action potentials. The relationship between the spike duration and the current amplitude is specific for each of the T‐type channels, reflecting their individual kinetic properties. Typically the charge transfer increases with spike broadening, but the total Ca 2 + entry saturates at different spike durations according to the channel type: 4 ms for α1G; 7 ms for α1H; and > 10 ms for α1I channels. During bursts, currents are inhibited and/or transiently potentiated according to the α1 channel type, with larger effects at higher frequency. The inhibition may be induced by voltage‐independent transitions toward inactivated states and/or channel inactivation through intermediate closed states. The potentiation is explained by an acceleration in the channel activation kinetics. Relatively fast inactivation and slow recovery limit the ability of α1G and α1H channels to respond to high frequency stimulation ( > 20 Hz). In contrast, the slow inactivation of α1I subunits allows these channels to continue participating in high frequency bursts (100 Hz). The biophysical properties of α1G, H and I channels will therefore dramatically modulate the effect of neuronal activities on Ca 2 + signalling.