Abstract

Fos protein expression has been used to reflect neuronal activation in pain processing pathways although analgesics may uncouple behavioral and Fos responses. We determine whether formalin-induced spinal c- fos mRNA expression (Northern blotting) correlates with nocifensive behavior following pretreatment with morphine, the α 2-adrenoceptor agonist dexmedetomidine, or their respective antagonists naloxone and atipamezole. Both opiate and α 2-adrenoceptor agonists reduced formalin-induced c- fos gene transcription and nocifensive behavior via their cognate receptors. Unexpectedly, blockade of either the opiate or α 2-adrenergic receptors, alone, caused an increase in formalin-evoked c- fos mRNA; while blocking the opiate receptor had no effect on formalin-induced behavior, α 2-adrenoceptor block had an analgesic effect, indicating discordance between c- fos message transcription and nocifensive behavior. We concluded that the formalin-induced spinal c- fos signal was a poor predictor of the behavioral response to pharmacological manipulation of pain processing pathways.

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