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The Journal of Neurophysiology Vol. 84 No. 1 July 2000, pp. 133-138
Copyright ©2000 by the American Physiological Society
1Department of Biomedical Engineering, Case Western Reserve University, Cleveland, Ohio 44106; and 2Department of Physiology and Biophysics and Department of Ophthalmology, Dalhousie University, Halifax, Nova Scotia B3H 4H7 Canada
Kourennyi, Dmitri E. and
Steven Barnes.
Depolarization-Induced Calcium Channel Facilitation in Rod
Photoreceptors Is Independent of G Proteins and Phosphorylation. J. Neurophysiol. 84: 133-138, 2000. Depolarization-induced facilitation of L-type Ca channels in
rod photoreceptors was investigated with nystatin-perforated and
ruptured whole cell patch-clamp techniques in cells isolated from tiger
salamander retina. Induction of facilitation was voltage dependent with
a half-maximal effect seen at prepulse potentials near +31 mV. Reversal
of facilitation was time dependent with fast (
20 ms)
and slow (
1 s) components at
60 mV. Incubation of
cells with pertussis toxin or intracellular administration of guanosine
5'-O-(3-thiotriphosphate) or guanosine 5'-O-(2-thiodiphosphate) had no effect on the degree to
which facilitation could be evoked, implying the absence of a
significant role for G proteins. Application of the phosphatase
inhibitor okadaic acid or inclusion of ATP, to boost levels of
phosphorylation, or inclusion of 5'adenylylimidophosphate or inhibitors
of protein kinase in the pipette, to reduce levels of phosphorylation,
had no effect on the development of facilitation, suggesting that phosphorylation has little or no role in this phenomenon. These results
show that the L-type Ca channels in rod photoreceptors, which appear to
be composed of
1F-like subunits, undergo
voltage-dependent facilitation in a manner that differs from some other
L-type Ca channels which undergo facilitation via phosphorylation or
through G-protein-mediated inhibition.
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