The cervical facet joint and its capsule have been identified as a common source of chronic neck pain from whiplash and have been reported to be injured during whiplash scenarios. Both the metabotropic glutamate receptor 5 (mGluR5) and the excitatory amino acid carrier 1 (EAAC1) have pivotal roles in chronic pain. In this study, spinal mGluR5 and EAAC1 were quantified following painful facet joint distraction in a rat model of facet-mediated painful loading, and were evaluated for their correlation with the severity of capsule loading. Rats underwent either a dynamic C6/C7 joint distraction simulating loading experienced during whiplash (distraction; n=12) or no distraction (sham; n=6) to serve as control. The severity of capsular loading was quantified using strain metrics, and mechanical allodynia was assessed after surgery. Spinal cord tissue was harvested at day 7 and the expression of mGluR5 and EAAC1 were quantified using western blot analysis. Mechanical allodynia following distraction was significantly (p<0.001) higher than sham. Spinal expression of mGluR5 was also significantly (p<0.05) greater following distraction relative to sham. However, spinal EAAC1 was significantly (p=0.0003) reduced compared to sham. Further, spinal mGluR5 expression was significantly positively correlated to capsule strain (p<0.02) and mechanical allodynia (p<0.02). Spinal EAAC1 expression was significantly negatively related to one of the strain metrics (p<0.003) and mechanical allodynia at day 7 (p=0.03). These results suggest that the spinal glutamatergic system may potentiate the persistent behavioral hypersensitivity that is produced following dynamic whiplash-like joint loading; chronic whiplash pain may be alleviated by blocking mGluR5 expression and/or enhancing glutamate transport through the neuronal transporter EAAC1.