Bodily injury in Aplysia, as in mammals, produces long-lasting memory traces at various neural loci. One consequence of injury, damage to peripheral axons, produces long-term hyperexcitability, synaptic facilitation, and growth in Aplysia sensory neurons. Similar effects are induced in these cells by repeated exposure to 5-HT that is released during aversive learning. An interesting question is to what extent cellular pathways that mediate the effects of axonal injury and 5-HT overlap. One current focus is on identifying cytoplasmic signals that initiate persistent sensory alterations that contribute to both long-term sensitization and memory of injury.