Preprodynorphin (
PPD) and
preproenkephalin (PPE) gene expression in a rat model of orofacial
inflammation were examined in order to further characterize the neurochemical mechanisms underlying orofacial
inflammation and
hyperalgesia. Deep and cutaneous orofacial
inflammation was produced by a unilateral injection of complete
Freund's adjuvant (CFA) into the rat temporomandibular joint (TMJ) or perioral skin (PO), respectively.
RNA blot analysis of the tissues including the spinal trigeminal complex revealed that the
PPD mRNA level ipsilateral to TMJ
inflammation was increased by 56.5+/-14.7% (n=4) when compared to the Naive group, and was significantly greater than the contralateral
PPD mRNA level (p<0.05). The distribution of neurons that exhibited
PPD mRNA after
inflammation was localized by in situ hybridization (naive approximately 0). In TMJ-inflamed rats (n=6)
PPD mRNA-positive neurons were found ipsilaterally in the medial portion of laminae I-II of the upper cervical dorsal horn (4.5+/-0.3), the dorsal portion of the subnucleus caudalis and caudal subnucleus interpolaris (5.2+/-0.3), and the paratrigeminal nucleus (6.4+/-1.2). A very localized induction of
PPD mRNA was also identified in a group of neurons in the intermediate portion of the subnucleus caudalis (2.4+/-0.4) in PO-inflamed rats (n=6). The distribution of these
PPD mRNA-positive neurons was somatotopically relevant to the site of injury. There were no significant changes in PPE
mRNA expression in both TMJ- and PO-inflamed rats. These results indicate that TMJ
inflammation resulted in a more intense and widespread increase in
PPD mRNA expression when compared to PO
inflammation. These changes may contribute to persistent central hyperexcitability and
pain associated with
temporomandibular disorders.