Neck pain commonly results from whiplash injury and has a high incidence, with staggering annual costs. Although the cervical facet joint has been identified as a source of neck pain, the cellular mechanisms that initiate and maintain pain from facet joint injury are unclear. The facet capsule is innervated with nociceptive afferents that can be activated in response to stretch during whiplash injury. This thesis uses a rat model of facet joint distraction to investigate the contributions of spinal inflammation and aspects of neuronal plasticity to facet-mediated pain. In particular, since glutamate receptors and transporters are critical in maintaining cellular homeostasis, their temporal response is quantified in both the dorsal root ganglion and spinal cord following joint distractions that do and do not produce behavioral hypersensitivity. In addition, the contribution of one aspect of spinal neuronal function to persistent pain in this model is evaluated by blocking a subunit of the voltage-gated calcium channel. In response to joint injury, inflammatory mediators, such as prostaglandins and cytokines, can be released in the periphery and the spinal cord. Accordingly, selective blocking of cytokine signaling in the injured joint or the spinal cord is performed to determine the peripheral and central contributions of pro-inflammatory cytokines to persistent behavioral hypersensitivity. Additional studies examine the role of prostaglandin synthesis in the painful facet joint via treatment with a non-steroidal anti-inflammatory drug. Finally, despite evidence of inflammation in pain and a known relationship between inflammation and activation of the integrated stress response (ISR), the contribution of the neuronal stress response to pain is undefined. As such, aspects of the ISR were quantified in dorsal root ganglion neurons for facet distractions with and without sensitivity to begin to define the role of the ISR in the maintenance of joint pain. Overall, this work demonstrates that behavioral hypersensitivity produced by excessive facet capsule stretch simulating whiplash can be initiated and sustained though the coordinated interplay of neuronal and inflammatory mediators in the nervous system. This thesis establishes the foundation for understanding the molecular mechanisms by which mechanical joint injury leads to the maintenance of facet-mediated pain.