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Plasticity in the circuits for the withdrawal reflexes has been correlated with several simple forms of nonassociative and associative learning in Aplysia, and biochemical, biophysical, and molecular mechanisms of plasticity in these circuits have been described. In order to examine network features of this plasticity, we identified and characterized a component of the modulatory circuitry for the tail- siphon withdrawal circuit. Activation of mechanoafferent neurons in the J cluster of the cerebral ganglion produced strong and distributed input to the tail-siphon withdrawal circuit. Stimulation of the J cells led to excitatory and inhibitory effects in the sensory neurons in the pleural ganglion, the tail motor neurons in the pedal ganglion, and several classes of interneurons in the pleural ganglion, including the multifunctional neuron LPI17. Activation of the J cells produced both fast and slow post-synaptic potentials in neurons of the tail-siphon withdrawal circuit. Of particular interest was the ability of the J cells to produce slow EPSPs in the pleural sensory neurons. These slow EPSPs were associated with an increase in the excitability of the sensory neurons, but no effect of the J cells on spike duration in the sensory neurons was observed. The J cells appear to mediate both sensory and modulatory inputs to the circuit for tail withdrawal.

Distributed input to the tail-siphon withdrawal circuit in Aplysia from neurons in the J cluster of the cerebral ganglion