Introduction:
    While synapses between neurons have been shown to display mechanisms for memory, axons have primarily been viewed as a conductor cable, simply relaying messages, without having any real effect on memory. Zimmerman's past study (as cited in Weragoda, Ferrer, & Walters, 2004), however, has shown that mammalian sensory axons can display persistent hyperexcitability at sites of nerve injury.
      In this study, neurons extracted from Aplysia, a type of marine mollusk, showed long term hyperexcitability (LTH) in both tail sensory and a giant secretomotor neuron (R2) after the connected axon was severed. Also, the axon of the tail sensory and tail motor neurons, but not the R2 secretomotor neuron, showed localized LTH after depolarization was induced by flooding the neuron with extracellular Potassium. Both the induction and expression of these types of LTH were prevented by the presence of protein synthesis inhibitors, anisomycin and rapamycin. Past studies conducted by Martin (2000), Martin et. al. (2000), Kandel (2001), and Jiang and Schuman (2002) (as cited in Weragoda, Ferrer, & Walters, 2004) show that the three features displayed by the tested Aplysia axons, "long-term changes in synapses caused by depolarization, restriction of the changes to intensely depolarized regions, and dependence of alterations on protein synthesis" were already found to be features in various synaptic models that are important to memory formation. This leads to the possibility that axons which have these three features might play a role in memory formation and provide insight to the early evolution of memory mechanisms.


Discussion:
    The findings from this study seem to support the hypothesis that axons could play a role in learning through the link between injury responses and memory mechanisms.
    Through the nerve crush, the study showed, "LTH was expressed reliably as a decrease in axonal spike threshold" (Weragoda, Ferrer, & Walters, 2004). A long-term decrease in the spike threshold was also observed during induced depolarization.. "By subjecting an axon to prolonged shock for 2 minutes or placing it in a high potassium saline solution for 2 minutes was enough to induce localized LTH. This suggests that axonal depolarization acts as a primary signal for inducing local LTH during nerve injury" (Weragoda, Ferrer, & Walters, 2004).  The induction of protein synthesis caused the spike threshold to increase in axons that were either crushed or depolarized. For axons that were not treated or injured, the induction of protein synthesis had no effect. "This indicates that depolarization or injury would cause a long-lasting decrease in excitability if protein synthesis were absent at the time of treatment, suggesting that the LTH has compensatory as well as sensitizing functions in regulating excitability" (Weragoda, Ferrer, & Walters, 2004). Supporting this finding is a past study done by Martin et. al. (as cited in (Weragoda Ferrer, & Walters 2004) which found that protein synthesis can occur in adult axons of Aplysia sensory neurons.
    The decrease in the spike threshold caused by depolarization is important when considering the evolution of Aplysia.  The decrease in the spike threshold should counteract the probability of conduction failure that occurs in an injured region. Aplysia's ancestors were soft-bodied animals whose axons were prone to injury.  
    Also worth noting are past studies conducted by Woollacott and Hoyle (1977), Brons and Woody (1980), Crow and Alkon (1980), Disterhoft et. al (1986), Scholz and Bryne (1987) and Walters (1987) (as cited in Weragoda, Ferrer, & Walters, 2004) for finding "neuronal LTH to be on of the first correlates of learning reported in invertebrates and vertebrates".  Since hyperexcitability itself might contribute to memory, LTH in Aplysia axons might also play a role in memory formation.