Traumatic neck injuries commonly result from rear-end motor vehicle collisions and are associated with a high incidence of neck pain and considerable annual costs. The facet joint is the most common source of neck pain. That joint is innervated by nociceptors that are activated by tensile stretching of the joint's capsular ligament. Although activation of those joint afferents and joint inflammation contribute to facet-mediated pain, the cellular response(s) within the joint that initiate pain via the joint afferents are unknown. Similarly, the mechanisms that induce central sensitization and maintain facet pain are not fully defined. Nerve growth factor (NGF) is a potent mediator of inflammatory cascades and is hypothesized to contribute to joint pain. Further, NGF regulates brain-derived neurotrophic factor (BDNF), which, when released in the spinal cord, sensitizes spinal neurons. Despite their roles in inflammatory pain, no studies have identified whether the neurotrophins NGF and/or BDNF contribute to facet joint-mediated pain. These studies utilize a rat model of mechanical facet joint injury to investigate the roles of NGF and BDNF in facet pain. Because joint afferents are crucial for the initiation and maintenance of facet pain, the innervation pattern of the C6/C7 facet joint in the rat is quantitatively defined. NGF expression is measured in the facet joint and the dorsal root ganglion (DRG) following a painful facet joint distraction. Further, the role of intra-articular NGF in the initiation and maintenance of facet-mediated pain and spinal neuronal hyperexcitability is evaluated by selectively blocking intra-articular NGF signaling. BDNF expression is quantified in the DRG and spinal cord after joint injury. Selective inhibition of spinal BDNF is utilized to determine its contribution to facet-mediated pain. This thesis demonstrates that throughout the peripheral and central nervous systems neurotrophins are key mediators of behavioral hypersensitivity and contribute to the hyperexcitability of spinal neurons after a painful facet joint injury. This work further establishes the need for future studies to integrate investigations throughout all aspects of the pain pathway to fully understand the mechanisms underlying facet-mediated pain.