Central neuronal mechanisms of siphon withdrawal in Aplysia were studied for the first time in intact, freely behaving animals by means of population recordings from implanted whole-nerve cuff electrodes. Intracellular follow-up studies were then conducted when the same animal was reduced to a semi-intact preparation. 2. Background spontaneous activity in the siphon nerve consisted of low-frequency firing of a population of efferent units containing identified siphon motoneurons. 3. Spontaneous patterned bursts of efferent activity occurred irregularly and were associated with all-or-nothing contractions of the parapodia, gill, and siphon. Spontaneous bursts were due to centrally generated activity in the interneuron II (INT II) network, an oscillatory network with endogenous pacemaker properties. 4. In intact animals, even weak tactile stimuli to the siphon typically triggered an INTII burst shortly after the stimulus-locked efferent activity. Thus, the stimulus can phase-advance the INT II oscillator. In semi-intact preparations, short-latency INT II bursts were triggered less less frequently and required more intense stimuli. 5. With weak to moderate-intensity stimuli in intact animals, the presence of short-latency triggered INT II bursts largely determined the duration of the siphon component and amplitude of the gill component of the withdrawal reflex. 6. When stimuli were repeated over a range of interstimulus intervals (from 60 to 1 min), the likelihood of triggering a short-latency INT II burst die not change systematically. Thus, the ability of the siphon stimulus to stably entrain the all-or-none INT II component over a wide range of intervals will interact behaviorally with the decrement of the monosynaptic component of the reflex with repetition.
