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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)

The involvement of bulbospinal pathways in fentanyl-induced inhibition of spinal withdrawal reflexes in the decerebrated rabbit.

The selective opioid OP3(mu)-receptor agonist fentanyl was administered via the intravenous, intrathecal and intraventricular routes to decerebrated rabbits in doses from 1-30 microg/kg. Reflexes evoked in medial gastrocnemius motoneurones by electrical stimulation of the sural nerve were depressed by fentanyl given by all three routes. The opioid was most potent when given intrathecally and least potent when given into the fourth ventricle. Blockade of spinal alpha2-adrenoceptors by intrathecal RX 821002 (100 microg) reduced the effectiveness of intrathecal and low (<3 microg/kg) intravenous doses of fentanyl, but did not affect or enhanced responses to high intraventricular and intravenous doses. Spinalization reduced the effectiveness of intrathecal and intravenous fentanyl and abolished inhibition from intraventricular dosing. These data show that fentanyl acts in the spinal cord and in the brain stem to suppress spinal reflexes, although very high doses were required for effects from the latter site. It appears that low intravenous doses of fentanyl act mainly in the spinal cord and that increasing the dosage recruits descending inhibition. The results of alpha2-adrenoceptor blockade indicate that the spinal inhibitory effects of opioids are enhanced by an interaction with endogenous noradrenaline in the spinal cord. Thus, the full expression of the spinal inhibitory effects of fentanyl is dependent on brain stem cell groups, either as a source of noradrenaline input to the spinal cord, or as a site from which opioids can activate descending inhibitory systems.[1]


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