Abstract
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≈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.
Published Version
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