The
peptide FMRFamide (Phe-Met-Arg-Phe-NH(2)) is known to modulate the circadian pacemaker found in the eye of the marine snail
Bulla gouldiana. In the present study, we investigated the cellular mechanisms underlying this modulation by examining the effects of
FMRFamide on the membrane properties of the circadian pacemaker cells, known as basal retinal neurons in this preparation. Bath application of
FMRFamide (0.1-1 microM) increased the membrane conductance, and hyperpolarized the membrane potential of these neurons. Next, perforated-patch recordings were used to demonstrate that
FMRFamide reversibly increased the outward current amplitude due to an augmentation of a non-inactivating
calcium-independent current. Reversal potential of the tail currents and its dependence on extracellular
potassium concentration suggested
potassium ions as the charge carrier for this current. The
peptide-modulated outward current was blocked by 54% after bath application of the
potassium channel blocker tetraethylammonium chloride and completely blocked by substituting
cesium for intracellular
potassium. Voltage dependence, activation kinetics and tail current kinetics of the
FMRFamide-modulated current were consistent with values found for the delayed rectifier current.Overall, our data suggest that
FMRFamide modulates a delayed rectifier
potassium current and at least one other, less voltage-dependent conductance. This provides a mechanistic explanation for
FMRFamide's ability to both shift the phase and attenuate light-induced phase shifts of the circadian pacemaker in B. gouldiana.