Hypoalgesia following microinjection of noradrenergic antagonists in the nucleus raphe magnus

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Abstract
The influence of the noradrenergic input to the nucleus raphe magnus (NRM) on the capacity of this nucleus to modulate nociceptive threshold was investigated in rats by microinjection of noradrenergic (NA) antagonists in the NRM. The distribution of NA terminals associated with the NRM was visualized histochemically using a glyoxylic acid-induced fluorescence technique. Microinjection of 5.0 and 10.0 .mu.g phentolamine at sites within the NRM, which was densely innervated by NA terminals, produced a dose-related hypoalgesia assessed by tail flick and hot plate tests. Microinjection of these doses at sites close to yet outside the NRM, in areas less densely innervated with NA terminals, was ineffective or produced hypoalgesia after a substantial delay. Similar results were obtained following microinjection of 10.5 .mu.g azapetine, another NA antagonist. The correspondence between the distribution of NA terminals associated with the NRM and the distribution of active sites for hypoalgesia in this area suggests that hypoalgesia was caused by blockade of the NA input to the NRM. Those cells of the NRM involved in the modulation of nociceptive threshold are apparently subject to a tonic, inhibitory NA input, the suppression of which produces hypoalgesia.