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Both pre- and postsynaptic mechanisms have been proposed as an explanation of the depressive effects of opioids on the activity of nociceptive dorsal horn neurons. In order to gauge the importance of the two mechanisms, we studied the effect of morphine on the spontaneous hyperactivity of nociceptive dorsal horn neurons in the spinalized decerebrated deafferented rat (C5-Th1). In this preparation, intravenous morphine was shown to depress spontaneous firing rate in a dose-dependent fashion. A comparative analysis of the effect of the same dose of morphine (2 mg/kg i.v.) in the intact spinalized decerebrated arthritic rat, in which dorsal horn convergent neurons also display high spontaneous activity, revealed that systemic morphine is twice as potent when primary afferent fibers are left intact. These results can explain why the analgesic effect of morphine is more marked against pains due to an excess of nociception than against pains arising from deafferentation.
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Lombard et al. (1989) studied this question.
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