魚類黒色素胞の果粒凝集反応におよぼすモノアミン酸化酵素阻害剤およびピロガロールの影響

It is generally accepted that in many teleosts the melanophores are primarily controlled by the autonomic nervous system, and that the nerve functioning in pigment aggregation is sympathetic. Many physiological and pharmacological data have shown that the transmitter released from the nerve endings is adrenergic and that the receptor in the melanophore may be of the alpha nature (Fujii 1961, Scheline 1963. Scott 1965, Abbott 1968, Iga 1968a, Fujii and Novales 1969). No matter what nature of the neurotransmitter acting at the neuro-melanophoral junction may be, the neurotransmitter suffers finally enzymatic destruction and must be removed from the sites of action, after the released, active neurohumore reacted with the receptor and played some roles as a trigger of excitation.
Participation of the following two kinds of enzymes is thought to be important on the metabolism of catecholamines : one is monoamine oxidase (MAO) acting on deamination of the amines, and the other catechol-O-methyltransferase (COMT) catalyzing O-methylation of the catecholamines. It has been generally believed that O-methylation by COMT is the first and important step in mammals (Kopin and Axelrod 1963, Axelrod 1965, Nagatsu 1965, Yoshida 1966) : Inhibition of MAO activity generally failed to augment the effect of the catecholamine, but COMT inhibitors induced the augmentation of the effect of endogenous and exogenous adrenaline. However, Crout et al. (1961) have been reported that the relative significance of these two metabolic pathways probably varies considerably from organ to organ and from species to species. Furthermore, there are some reports that the action of tyramine is potentiated by the MAO inhibitors (Giersemer et al. 1953. Goldberg and Sjoerdsma 1959, Vanov 1962). The mechanism of tyramine potentiation after the treatment of MAO inhibitors is not always clear, because tyramine acts indirectly through release of endogenous catecholamines on the target cells.
On the other hand, on physiology of the fish melanophores, there is little information from the view point of the inactivation process of the transmitter substance except pharmacological studies of Scott (1965, 1968), who observed the potentiating effect of norepinephrine and epinephrine injected subcutaneously with pretreatment of pyrogallol, an inhibitor of catechol-O-methyltransferase, in the sand flounder Scopthalmus aquosus.
The present experiments were designed to examine whether the MAO inhibitors can modify the pigment aggregating effect of the endogenously released neurohumore and also exogenous adrenaline. Furthermore, the similar experiments were carried out with pyrogallol and the results were compared with those with MAO inhibitors. Thus, an atternpt was made to study the problem of inactivation of the pigment aggregating neurotransmitter in the fish melanophore and to ascertain the nature of the transmitter by an indirect pharmacological approach.