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1 Program in Neuroscience, 3 Program in Cellular and Molecular Physiology, 2 Department of Physiology, University of Massachusetts Medical School, Worcester, Massachusetts 01655
We recently reported that
arachidonic acid (AA) inhibits L- and N-type Ca2+ currents
at positive test potentials in the presence of the dihydropyridine L-type Ca2+ channel agonist (+)-202-791 in dissociated
neonatal rat superior cervical ganglion neurons [Liu L and Rittenhouse
AR. J Physiol (Lond) 525: 291-404, 2000]. In this
first of two companion papers, we characterized the mechanism of
inhibition by AA at the whole cell level. In the presence of either
-conotoxin GVIA or nimodipine, AA decreased current amplitude,
confirming that L- and N-type currents, respectively, were inhibited.
AA-induced inhibition was concentration dependent and reversible with
an albumin-containing wash solution, but appears independent of AA
metabolism and G protein activity. In characterizing inhibition, an
AA-induced enhancement of current amplitude was revealed that occurred
primarily at negative test potentials. Cell dialysis with albumin
minimized inhibition but had little effect on enhancement, suggesting
that AA has distinct sites of action. We examined AA's actions on
current kinetics and found that AA increased holding
potential-dependent inactivation. AA also enhanced the rate of N-type
current activation. These findings indicate that AA causes multiple
changes in sympathetic Ca2+ currents.
calcium channel; 5,8,1,14-eicosatetraynoic acid; FPL-64176; fatty acid; oleic acid
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