Since partial peripheral injury does not necessarily lead to the development of neuropathic pain it is possible that a set of genes is directly regulated by the development of neuropathic pain independent of the genes regulated by nerve injury. This study identifies the genes expressed within the spinal cord that are uniquely regulated by tactile allodynia in rats. Using subtractive methods, genes regulated by allodynia were differentiated from those of nerve injury. Gene ontology analysis identified that allodynic genes are involved in a variety of processes including myelination, actin cytoskeleton reorganization, dephosphorylation, phosphorylation, response to stress, as well as protein trafficking and RNA processing. The processes of protein trafficking and RNA processing were found to be as statistically significant as other processes that have been associated with neuropathic pain development such as response to stress, phosphorylation, and cell migration. Trafficking and transcription are linked and undergo activity dependent regulation which results in both rapid and gradual synaptic changes (plasticity). The data presented here greatly expand the list of genes regulated by the development of tactile allodynia and reveal protein trafficking and RNA processing as prominent biological processes that may be involved in synaptic plasticity changes within the spinal cord in response to allodynia.