CONTRIBUTION OF THE CAMP-DEPENDENT SIGNAL PATHWAY TO CIRCADIAN SYNCHRONY OF MOTILITY AND RESTING MEMBRANE-POTENTIAL IN PARAMECIUM

It is known that the ciliated protozoan Paramecium multimicronucleatum has synchronized circadian rhythms of motility, resting membrane pote ntial and cyclic adenosine 3',5'-monsphosphate (cAMP) and cyclic adeno sine 3',5'-monophosphate (cGMP) concentrations. The present study show s that (1) extacellularly added 4 mM tetraethylammonium (TEA)(+) (a K channel blocker) almost completely abolishes the diurnal oscillation of intracellular cAMP concentrations; (2) even 32 mM TEA(+) fails to a bolish the circadian motility rhythm; hot (3) the motility rhythm is h ighly damped when 4 mM TEA(+) and 100 mu M CdCl2 (a Ca2+ channel block er) are added simultaneously. A cAMP analogue (N-6-monobutyryl-cAMP) a dded extracellularly accelerates swimming velocity. Both a K+ channel blocker (e.g. TEA(+)) and an inhibitor (trifluoperazine) of adenylate cyclase (AC) suppress cAMP formation, supporting the hypothesis that A C in Paramecium has dual functions, as a K+ channel and as an enzyme f or cAMP formation. It is hypothesized that the circadian synchrony is due to circadian fluctuations of AG causing separate circadian changes both in ciliary motion and membrane potential through a cAMP-dependen t signal pathway that forms a sophisticated network of second messenge rs to govern the synchrony together with Ga2+ - and cGMP-dependent pat hways in a manner antiphasic and/or complementary to one another.