Pavlovian conditioning of Hermissenda produces both light-elicited inhibition of normal positive phototactic behavior and conditioned stimulus (CS)-elicited foot-shortening. Rotation, the unconditioned stimulus (US) elicits foot-shortening and reduced forward ciliary locomotion. The neural circuit supporting ciliary locomotion and its modulation by light is known in some detail. However the neural circuits responsible for rotation-elicited foot-shortening and reduced forward ciliary locomotion are not known. Here we describe components of the neural circuit in Hermissenda that produce anterior foot contraction and ciliary activation mediated by statocyst hair cells. We have characterized in semi-intact preparations newly identified pedal ventral contraction motor neurons (VCMNs) and interneurons (I_b). Type I_b interneurons receive polysynaptic input from statocyst hair cells and project directly to VCMNs and cilia activating motor neurons. Depolarization of VCMNs with extrinsic current in normal artificial seawater (ASW) and high-divalent cation ASW, and under conditions where central synaptic transmission was suppressed with 5 mM Ni²⁺ ASW, elicited a contraction of the ipsilateral anterior foot measured from videotape recordings. Mechanical displacement of the statocyst or depolarization of identified statocyst hair cells with extrinsic current elicited spikes and complex EPSPs in type I_b interneurons and complex EPSPs and spikes recorded in VCMNs. Type I_b interneurons are electrically coupled and project to VCMNs and VP1 cilia activating motor neurons located in the contralateral pedal ganglia. The results indicate that statocyst hair cell mediated anterior foot contraction and graviceptive ciliary locomotion involve different interneuronal circuit components from the circuit previously identified as supporting light modulated ciliary locomotion.