Effects of biogenic amines and psychotropic drugs on endogenous prostaglandin biosynthesis in the rat brain homogenates

Phenylalkylamine and indolalkylamine derivatives, as well as several drugs acting on the central nervous system, were tested for their effects on endogenous prostaglandin, (PG) biosynthesis in the rat brain homogenates. In the particulate suspension obtained by the removal of the soluble fraction from the rat brain homogenates PG-biosynthesis could be stimulated by noradrenaline. dopamine, adrenaline, serotonin, tryptamine and to a slight extent by tyramine. Isoprenaline, DOPA. α-methyl noradrenaline, α-methyl dopamine, α-methyl tryptamine and 5-hydroxy tryptophan were ineffective. PG-biosynthesis stimulated by catecholamines or indolalkylamines responsively could be inhibited by compounds with monoamine oxidase blocking properties. In the total rat brain homogenates another type of PG-biosynthesis could be demonstrated in the absence of catecholamine or indolalkylamine that could not, or but to a slight extent, be inhibited by monoamine oxidase blocking agents. Apomorphine, oxypertine, α-methyl noradrenaline, promethazine, DOPA, reserpine, chlorpromazine, desipramine, yohimbine and tetrabenazine inhibited this type of PG-biosynthesis, though they failed to influence PG-formation stimulated by catecholamine or indolalkylamine. A correlation could be established between the PG-formation inhibitory and lipid peroxidation antagonizing effects of these compounds. Non-steroidal anti-inflammatory agents, such as indomethacin, acetylsalicylic acid and dipyrone, inhibited both types of PG-biosynthesis. The results permit the conclusion that psychotropic drugs exert their effects on endogenous PG biosynthesis in the rat brain homogenates by inhibiting various activation processes.