Neural control of locomotion in Aplysia: Role of the Central Ganglia

Abstract

In this study the effects of connective lesions on the control of pedal locomotion in Aplysia californica were examined. Normal goal directed locomotion consists of a behavioral sequence. The foot is detached, extended, and the anterior edge reattached. A series of waves are generated in the resulting arch which pull the animal forward. Escape locomotion is similar except that the foot extension is exaggerated; the entire body contracts off the substrate and the tail is released following anterior foot attachment. When the cerebropedal and cerebropleural connectives were bilaterally sectioned, locomotion was abolished. Bilateral sectioning of the cerebropedal connectives alone also eliminated the first phases of normal locomotion, although limited pedal waves were still generated. Bilateral sectioning of the cerebropleural connectives only eliminated escape locomotion. Cutting the pleuropedal connectives greatly reduced the rate of normal locomotion and also abolished escape locomotion. Unilateral section of the cerebropedal and cerebropleural connectives resulted in reduced motor activity on the lesioned side, with diagonally running pedal waves (lesioned side trailing) in the foot. Sectioning the pedal commissure caused the motor activity of each hemifoot to become desynchronized. When the pedal ganglia were isolated by cutting both the cerebropedal and pleuropedal connectives limited pedal waves were still generated, although the initial phases of the locomotor sequence were absent. These results suggest that the different parts of the locomotor control system are localized in separate ganglia. The motor pattern generators reside in each pedal ganglion with coordination maintained by the pedal commissure. The results are consistent with the hypothesis that the commands for initiating locomotion originate in the cerebral ganglion and descend to the pedal ganglia via the cerebropedal connectives. The pleural ganglia apparently serve both to modulate the rate of locomotion and as a relay for input to the cerebral ganglion.