Orofacial deep and cutaneous tissue inflammation differentially upregulates preprodynorphin mRNA in the trigeminal and paratrigeminal nuclei of the rat
H. Imbe et K. Ren, Orofacial deep and cutaneous tissue inflammation differentially upregulates preprodynorphin mRNA in the trigeminal and paratrigeminal nuclei of the rat, MOL BRAIN R, 67(1), 1999, pp. 87-97
Preprodynorphin (PPD) and preproenkephalin (PPE) gene expression in a rat m
odel of orofacial inflammation were examined in order to further characteri
ze the neurochemical mechanisms underlying orofacial inflammation and hyper
algesia. Deep and cutaneous orofacial inflammation was produced by a unilat
eral injection of complete Freund's adjuvant (CFA) into the rat temporomand
ibular joint (TMJ) or perioral skin (PO), respectively. RNA blot analysis o
f 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 th
an the contralateral PPD mRNA Level (p < 0.05). The distribution of neurons
that exhibited PPD mRNA after inflammation was localized by in situ hybrid
ization (naive approximate to 0). In TMJ-inflamed rats (n = 6) PPD mRNA-pos
itive neurons were found ipsilaterally in the medial portion of laminae I-I
I of the upper cervical dorsal horn (4.5 +/- 0.3), the dorsal portion of th
e subnucleus caudalis and caudal subnucleus interpolaris (5.2 +/- 0.3), and
the paratrigeminal nucleus (6.4 +/- 1.2), A very localized induction of PP
D mRNA was also identified in a group of neurons in the intermediate portio
n of the subnucleus caudalis (2.4 +/- 0.4) in PO-inflamed rats (n = 6). The
distribution of these PPD mRNA-positive neurons was somatotopically releva
nt to the site of injury. There were no significant changes in PPE mRNA exp
ression 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 temporoman
dibular disorders. (C) 1999 Elsevier Science B.V. All rights reserved.