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Journal of Neuroscience, Vol 9, 3314-3325, Copyright © 1989 by Society for Neuroscience
Second messengers involved in the mechanism of action of bradykinin in sensory neurons in culture
GM Burgess, I Mullaney, M McNeill, PM Dunn and HP Rang
Sandoz Institute for Medical Research, London, United Kingdom.
Application of bradykinin to neonatal rat dorsal root ganglion neurons
caused a depolarization associated with an inward current and an increase
in membrane conductance that was probably due to the opening of sodium
channels. No hyperpolarization or outward current was detected. In
addition, bradykinin increased the rate of 45Ca uptake into the neurons by
a mechanism that was blocked by the dihydropyridine calcium channel
antagonist nifedipine. Direct activation of protein kinase C (PKC) with
phorbol esters mimicked the ability of bradykinin to depolarize the neurons
and to increase the rate of 45Ca uptake. Down- regulation of PKC by
prolonged treatment with phorbol esters and treatment of the cells with
staurosporine, which inhibits PKC, blocked both bradykinin- and phorbol
ester-induced 45Ca influx, and substantially reduced the proportion of
cells that gave electrophysiological responses to either agent. Bradykinin
also activated polyphosphoinositidase C in the dorsal root ganglion
neurons, elevating levels of inositol(1,4,5)-trisphosphate and 1,2-
diacylglycerol, an endogenous activator of PKC. It is suggested, therefore,
that PKC may mediate some of the effects of bradykinin in sensory neurons.
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