Abstract
The role of protein kinase C (PKC) activation in mediating muscarinic depolarization was assessed in the rat superior cervical ganglion. Staurosporine, an inhibitor of PKC, abolished a depolarization elicited by the direct PKC activator β-phorbol 12,13-dibutyrate, but had little effect on the response to muscarine. Thus, activation of PKC may not be an obligatory transduction step between muscarinic receptor stimulation and depolarization.
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