Abstract

The effects of FMRFamide and gamma-aminobutyric acid (GABA) on prey-capture reactions in Clione and on cerebral A and B neurons, which control opposite movements of prey capture appendages, have been studied. FMRFamide hyperpolarized A neurons and depolarized and increased spike activity in B neurons. FMRFamide thus had a reciprocal effect on A and B neurons, triggering buccal cone withdrawal. In addition, FMRFamide inhibited swimming, acceleration of which is a component of feeding arousal. Many neurons throughout the central nervous system showed FMRFamide immunoreactivity. Dense networks of immunoreactive fibers were localized in the head wall, buccal mass and in buccal cones, adjacent to striated longitudinal muscle cells. In wings, immunoreactive processes were found mainly in association with smooth retractor muscles. GABA depolarized and activated A neurons but hyperpolarized and inhibited B neurons. The overall effect of GABA thus resulted in extrusion of buccal cones. Both direct GABA responses and inhibitory postsynaptic potentials (IPSPs) induced in B neurons by A neuron activity were chloride-mediated. However, picrotoxin and bicuculline did not block IPSPs or direct GABA responses in B cells.

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