Similar neuronal alterations induced by axonal injury and learning in Aplysia.

Learning in the marine mollusk Aplysia has been associated with enhanced sensory function, expressed in mechanosensory neurons as (i) decreases in action potential threshold, accommodation, and afterhyperpolarization, and (ii) increases in action potential duration, afterdischarge, and synaptic transmission. These alterations also occur, with a delay, after sensory axons are injured under conditions in which synaptic transmission is severely reduced. The latency and specificity of injury-induced alterations indicate that induction signals are generated at the site of injury and conveyed centrally by axonal transport. Similarities in neuronal modifications support the hypothesis that some memory mechanisms evolved from mechanisms of injury-induced sensory compensation and repair.