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Abstract
This study examined the contribution of spinal δ 1 and δ 2 opioid receptors to the antinociception produced by microinjection of l-glutamate in either the nucleus raphe magnus (NRM) or the nucleus reticularis gigantocellularis pars α (NGCp α) of the rat. Intrathecal (i.t.) pretreatment with 1 μg of 7-benzylidinenaltrexone (BNTX), a δ 1 opioid receptor antagonist, did not antagonize the increase in tail flick latency (TFL) produced by microinjection of l-glutamate in either the NRM or the NGCp α. In contrast, i.t. pretreatment with 3 μg of naltriben (NTB), a δ 2 opioid receptor antagonist, completely antagonized the increase in TFL evoked by microinjection of l-glutamate in the NRM, but did not antagonize the increase in TFL evoked from the NGCp α. These results suggest that the antinociception produced by activation of these bulbospinal pathways is predominantly mediated by spinal δ 2 opioid receptors and that there is little, if any, contribution by spinal δ 1 opioid receptors.
Published Version
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