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Injury to the trigeminal nerves may cause maladaptive changes in synaptic connectivity that plays an important role in chronic pain development. Here we examined whether injury to the infraorbital nerve, a branch of the trigeminal nerves, led to synaptic ultrastructural changes when the injured animals have developed neuropathic pain states. Transmission electron microscopy was used to examine synaptic profiles in Vc\/C2 at 3 weeks postinjury, corresponding to the time of peak behavioral hypersensitivity following chronic constriction injury to the infraorbital nerve (CCI\u2010ION). Using established criteria, synaptic profiles were classified as associated with excitatory (R\u2010), inhibitory (F\u2010), and primary afferent (C\u2010) terminals. Each type was counted within the superficial dorsal horn of the Vc\/C2 and the means from each rat were compared between sham and injured animals; synaptic contact length was also measured. The overall analysis indicates that rats with orofacial pain states had increased numbers and decreased mean synaptic length of R\u2010profiles within the Vc\/C2 superficial dorsal horn (lamina I) 3 weeks post\u2010CCI\u2010ION. Increases in the number of excitatory synapses in the superficial dorsal horn of Vc\/C2 could lead to enhanced activation of nociceptive pathways, contributing to the development of orofacial pain states. J. Comp. 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