The capacity of the axon to locally synthesize proteins has now been shown to be critical for successful regeneration following injury. Once regeneration has occurred, how does the axon return to a “normal” state (i.e., how does a newly regenerated axon alter the transport and local translation of mRNAs back to the pre-injured state)? If this return to a pre-injured condition does not occur, what are the physiological consequences of this failure in terms of maladaptive plasticity and conditions such as neuropathic pain? The central hypothesis of this study is that changes in local protein synthesis in sensory axons alter the neuron’s capacity for propagating noxious stimuli. Our objective is to understand how axonal transport and local protein synthesis contribute to hyperexcitability exhibited by damaged neurons leading to neuropathic pain states. Current animal models of nerve trauma have provided some insights into the neuronal changes that occur in response to peripheral nerve damage - revealing a remarkable degree of plasticity in both the sensory neurons and spinal cord. Understanding how axonal transport and local protein synthesis contribute to increased hyperexcitability of these damaged sensory neurons may point to alternative methods of treating pathological pain states.