Trans-synaptic regulation of calmodulin gene expression after experimentally induced orofacial inflammation and subsequent corticosteroid treatment in the principal sensory and motor trigeminal nuclei of the rat.

The cutaneous and mucosal surfaces in the infraorbital region around the whisker pad are innervated by the maxillary division of the afferent fibers of the trigeminal nerve, while certain ganglion cells project to the principal sensory trigeminal nucleus (Pr5). In turn, some of the neurons in the Pr5 project to the motor trigeminal nucleus (Mo5), whose neurons do not innervate the infraorbital skin. We analyzed the calmodulin (CaM) gene expression in these nuclei after dithranol-induced inflammation and subsequent treatment with corticosteroid in the infraorbital skin. CaM gene-specific mRNA populations were detected through quantitative image analysis of the distribution of CaM gene-specific riboprobes in brain stem cryostat sections of control rats and rats chronically treated with dithranol, corticosteroid or both. These nuclei displayed a differentially altered CaM gene expression in response to the treatments. While the CaM I and II mRNA contents were increased, the CaM III transcripts remained unaltered after chronic dithranol treatment in the Mo5. In the Pr5, however, the CaM mRNA contents were either unchanged (CaM I and III) or increased (CaM II). Subsequent corticosteroid treatment reversed the stimulatory effects of dithranol on the expression of all the CaM genes in the Mo5, but was without significant effects on the CaM I and II genes, or even increased the CaM III mRNA contents in the Pr5. Corticosteroid treatment alone was either ineffective or decreased the levels of CaM mRNAs in these nuclei. These data suggest that peripheral noxae of dermal origin may result in a trans-synaptically acting differential regulation of the multiple CaM genes in the brain.