Mechanisms underlying the effects of amphetamine on particulate PKC activity.

Amphetamine stimulates particulate protein kinase C (PKC) activity that is associated with the outward-transport of dopamine (DA) (Giambalvo [2003] Synapse 49:125-133). This stimulatory effect requires intracellular calcium ([Ca](i)) and endogenous DA and when DA release is diminished, the inward-transport of amphetamine inhibits PKC activity. This study examines the mechanisms involved.

Effects of fenfluramine and antidepressants on protein kinase C activity in rat cortical synaptoneurosomes.

Fenfluramine releases serotonin (5-HT) via the 5-HT transporter (SERT). Previous work has shown that amphetamine increases particulate protein kinase C (PKC) activity in striatal synaptoneurosomes. The increased PKC activity is linked to the outward transport of dopamine, and when release is diminished, the inward transport of amphetamine inhibits PKC instead.

Differential effects of amphetamine transport vs. dopamine reverse transport on particulate PKC activity in striatal synaptoneurosomes.

Amphetamine has been shown to increase striatal particulate protein kinase C (PKC) activity [Giambalvo (1992b) Neuropharmacology 31:1211-1222]. The present study examined possible mechanisms involved. Specifically, the effects of calcium, endogenous DA, and DA receptors on the amphetamine-induced increase in PKC activity in striatal synaptoneurosomes were examined.