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 beta-adrenergic receptor. We suppose that TCA-induced activation of PKC may be associated, at least in part, with the mechanism of TCA.


CONCLUSIONS
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.
Department of Psychiatry, Kawasaki Medical School, 577 Matsushima, Kurashiki City 701-0192, Japan. morisita@med.kawasaki-m.ac.jp
Shigeru
S
Morishita
Shozo
S
Aoki
D000368:Aged; D000818:Animals; D000929:Antidepressive Agents, Tricyclic / Q000494:pharmacology*; D001792:Blood Platelets / Q000187:drug effects / Q000201:enzymology*; D015536:Down-Regulation; D005260:Female; D006801:Humans; D007273:Injections, Intramuscular; D008297:Male; D008875:Middle Aged; D018377:Neurotransmitter Agents / Q000493:pharmacokinetics; D011493:Protein Kinase C / Q000187:drug effects / Q000494:pharmacology*; D011817:Rabbits; D011943:Receptors, Adrenergic, beta / Q000187:drug effects / Q000502:physiology; D015398:Signal Transduction
D000929:Antidepressive Agents, Tricyclic; D018377:Neurotransmitter Agents; D011943:Receptors, Adrenergic, beta; D011493:Protein Kinase C