Sedation induced by reserpine has been considered “true” sedation because anesthesia or loss of the righting reflex is never produced by reserpine even in very large doses [Berger, 1957 (1)]. Reserpine might be a serotonin liberator and its central actions are attributed to the liberated serotonin [Brodie, et al. 1957 (2)]. On the other hand, lysergic acid diethylamide (LSD), a specific psychotomimetic agent, is well known as a potent inhibitor of serotonin [Gaddum, 1953 (3)]. Actually, LSD not only blocks the reserpine-induced sedation, but also inhibits the potentiating effect of reserpine on barbiturate hypnosis in mice [Brown, 1957 (4)]. Burton (1957) (5) found that both LSD and amphetamine have a selective analeptic action on the reserpine-sedation among various kinds of agents including central stimulants or autonomic blocking agents. According to Teschler and Cerletti (1957) (6), reserpine is rather a potentiator of the central stimulatory action of LSD.
Kumagai and Yui (1950) (7) reported on the general pharmacology of agroclavine and dihydroagroclavine which Abe and his collaborators (1951) (8) had newly isolated from the saprophytic culture of a certain ergot fungus. Agroclavine caused some characteristic symptoms with central excitation, while dihydroagroclavine drowsiness as a sign of central depression. Recenty, Abe (1956) (9) has obtained a lot of derivatives of ergot alkaloids, the so-called “agroclavine-type” compounds (illustrated in Table 1), by means of cultural and chemical procedures.
This paper is concerned with the central action of these compounds, with special reference to their reserpine-antagonism.