Monoaminergic mechanisms associated with control of luminescence and contractile activities in the coelenterate, Renilla köllikeri

The effects of monoamines and adrenergic drugs on luminescent responses and rachidial contractions were investigated in the colony of the sea pansy Renilla köllikeri. Of several transmitter candidates tested, only adrenaline induced localized, phasic luminescence at low concentrations. Propranolol (1 mM) depressed adrenaline-induced and suppressed electrically stimulated luminescence, the latter being also abolished by 6-hydroxydopamine (6-OHDA) and reserpine. Desmethylimipramine (DMI, 20 μM), an uptake inhibitor of adrenergic neurons, potentiated luminescent responses to both adrenaline and electrical stimulation, and induced luminescence at higher concentrations. Pargyline, a monoamine oxidase inhibitor, produced DMI-like effects. Rachidial contractions in Renilla are biphasic events which are usually spontaneous and rhythmic, or can be induced by electrical stimulation. Noradrenaline and adrenaline enhanced the second phase of ongoing rhythmic contractions, but failed to induce contractions. Reserpine and 6-OHDA abolished electrically stimulated luminescence, but reserpine further depressed evoked contractions while 6-OHDA failed to affect rhythmic or evoked contractions. DMI (0.5 mM) initiated rhythmic contractile activity in quiescent preparations. These observations suggest that adrenaline or an as yet unidentified catecholamine may be involved as a neurotransmitter in luminescence control. Noradrenaline and/or adrenaline act possibly as neuromodulators for rachidial contractions in the sea pansy.