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Journal of Neuroscience, Vol 15, 6069-6076, Copyright © 1995 by Society for Neuroscience
Enhancement of high threshold calcium currents in rat primary afferent neurons by constitutively active protein kinase C
KE Hall, MD Browning, EM Dudek and RL Macdonald
Department of Internal Medicine, University of Michigan, Ann Arbor 48109, USA.
Protein kinase C has been implicated in the modulation of calcium channel
function. However, controversy exists concerning the actions of agents such
as phorbol esters or diacylglycerol (DAG) that activate endogenous PKC,
with both enhancement and inhibition of Ca2+ currents described. In this
article we report the effects of direct intracellular application of a
constitutively active form of PKC (PKM) on whole cell calcium currents in
acutely dissociated rat dorsal root ganglion neurons. PKM application
significantly enhanced high threshold voltage-activated calcium currents
elicited from holding potentials of - 80 mV and -40 mV. The rate of current
rundown in PKM-treated cells was not significantly different from controls.
The enhancement observed with PKM was not due to a shift in the voltage
dependence of the peak current. Synthetic PKC inhibitor peptide (PKC-I)
added to recording solutions containing PKM (PKM+PKC-I) abolished the
PKM-associated enhancement. The rate of current rundown was significantly
increased in the presence of PKM+PKC-I, and PKC-I alone, suggesting that
substantial enhancement of voltage-activated calcium currents by endogenous
PKC occurred in this preparation of rat dorsal root ganglion neurons. The
portions of current attributable to N-, L-, and non-N,L-type currents
[determined by applying the N- and L-type calcium antagonists omega-
conotoxin GVIA and nifedipine (3-10 microM)] were not affected by PKM,
suggesting that both N and L current components were enhanced by
PKM.(ABSTRACT TRUNCATED AT 250 WORDS)
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