title: Recovery of escape locomotion following a CNS lesion in Aplysia.
abstract: The recovery of escape locomotion in Aplysia following a CNS lesion was investigated. The connectives between the cerebral and pleural ganglia were crushed in anesthetized animals, producing a specific behavioral deficit. Animals with lesions failed to initiate escape locomotion in response to tail shock. Tail withdrawal and inking which were also evoked by tail shock were still present. Other behaviors such as normal locomotion and feeding were not impaired. There was gradual recovery from the effects of the lesion. Animals with lesions began to respond to tail shock with weak pedal waves at long latencies after 7-13 days. The responses grew more vigorous and the latencies decreased over subsequent days. Full escape locomotor responses were observed as early as 15 days postlesion. By Postlesion Day 27, all of the animals had completely recovered and gave full escape responses. The mean latency of the escape locomotor response in recovered animals was not significantly different from prelesion control values. In behaviorally recovered animals, retrograde tracing from a point distal to the lesion site stained neurons in the cerebral ganglion. Intracellular dye injections of individual neurons revealed sprouting of new processes. Stimulation of the tail nerve and individual neurons demonstrated synaptic connections between cerebral and pleural ganglia neurons. These results suggest that the observed behavioral recovery was due to pleural ganglia neurons regenerating and forming appropriate synaptic connections in the cerebral ganglion.
authors.affiliation: Department of Physiology, Meharry Medical College, Nashville, Tennessee 37208.
authors.forename: S M
authors.initials: SM
authors.lastname: Fredman
mesh_terms: D000818:Animals; D001048:Aplysia / Q000502:physiology*; D002490:Central Nervous System / Q000502:physiology*; D004597:Electroshock; D004924:Escape Reaction; D008124:Locomotion; D009416:Nerve Regeneration; D009475:Neurons, Afferent / Q000502:physiology