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1 Department of Pharmacology, University of Virginia School of Medicine, Charlottesville, Virginia 22903; 2 Department of Molecular Physiology and Biophysics, Vanderbilt University, Nashville, Tennessee 37232; 3 Laboratory of Molecular and Cellular Neuroscience, Rockefeller University, New York, New York 10021; and 4 Center for Bio/Molecular Science and Engineering, Naval Research Laboratory, Washington, District of Columbia 20375
The effect of
Ca2+/calmodulin-dependent protein kinase II (CaMKII)
stimulation on unitary low voltage-activated (LVA) T-type Ca2+ channel currents in isolated bovine adrenal
glomerulosa (AG) cells was measured using the patch-clamp technique. In
cell-attached and inside-out patches, LVA channel activity was
identified by voltage-dependent inactivation and a single-channel
conductance of ~9 pS in 110 mM BaCl2 or
CaCl2. In the cell-attached patch, elevation of bath
Ca2+ from 150 nM to 1 µM raised intracellular
Ca2+ in K+-depolarized (140 mM) cells and
evoked an increase in the LVA Ca2+ channel probability of
opening (NPo) by two- to sixfold. This augmentation was associated with an increase in the number of nonblank
sweeps, a rise in the frequency of channel opening in nonblank sweeps,
and a 30% reduction in first latency. No apparent changes in the
single-channel open-time distribution, burst lengths, or openings/burst
were apparent. Preincubation of AG cells with lipophilic or peptide
inhibitors of CaMKII in the cell-attached or excised (inside-out)
configurations prevented the rise in NPo elicited by elevated Ca2+ concentration.
Furthermore, administration of a mutant recombinant CaMKII
exhibiting cofactor-independent activity in the absence of elevated
Ca2+ produced a threefold elevation in LVA channel
NPo. These data indicate that CaMKII activity is
both necessary and sufficient for LVA channel activation by
Ca2+.
glomerulosa cells; low voltage-activated channels
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