The eyes of certain marine gastropods including Aplysia and
Bulla, contain circadian pacemakers, which produce a circadian rhythm of autogenous compound action potential (CAP) activity. The CAPs are generated by the synchronous spike discharge of a distinctive population of
retinal pacemaker neurons whose axons convey the CAP activity to the CNS. When CAP activity is recorded from a preparation with eyes attached to the CNS, the CAP activity is modulated by efferent activity. In this study we have identified
FMRF-amide-like immunoreactive efferent axons in the optic nerves of
Bulla. These axons arborize in the basal
retinal neuropil adjacent to the pacemaker neurons and are in a position to make synaptic contacts with their dendrites. Similar immunoreactive fibers are not observed in Aplysia eyes. Exogenous
FMRF-amide at micromolar concentrations suppresses ongoing CAP activity in isolated eyes but does not suppress the ERG or phase shift the circadian rhythm of CAP activity. Intracellular recordings from the
retinal pacemaker neurons reveal that
FMRF-amide hyperpolarizes the membrane potential, suppresses spike discharge, and decreases the input resistance, suggesting that a K conductance is increased. Electrical stimulation of the region of the cerebral
ganglion that contains
FMRF-amide immunoreactive neurons suppresses ongoing CAP activity. All these results are consistent with the idea that the
FMRF-amide immunoreactive central neurons and their axons provide a pathway for efferent modulation of the CAP rhythm generated by the
retinal pacemaker neurons.