Effects of tricyclic antidepressants on protein kinase C activity in rabbit and human platelets in vivo

Background: The purpose of this study was to examine the effects of tricyclic antidepressants (TCA) on protein kinase C (PKC) in vivo. Methods: PKC activity in rabbit and human platelets in vivo was measured after administration of TCA and in controls. Results: Administration of TCA increased PKC activity in rabbit and human platelets in vivo. Conclusions: It has been reported that activation of PKC mediates inhibition of neurotransmitter uptake and down-regulation of β-adrenergic receptor. We suppose that TCA-induced activation of PKC may be associated, at least in part, with the mechanism of TCA. Limitations: Other signal transduction systems, such as those of protein kinase A, protein kinase G, and cyclic-AMP, also affect neurotransmitter uptake and/or down-regulation. In this study, the relationship between the TCA–PKC system and other signal transduction systems was not investigated.