The role of 5-hydroxytryptamine (5-HT) in morphine-induced antinociception was evaluated in mice and rats by means of the specific 5-HT uptake inhibitor citalopram. Systemic and subarachnoidal administration of the compounds was made and then the animals were tested in the grid-shock and hot plate model. In non-antinociceptive doses, systemically and subarachnoidally administered citalopram potentiated the effect of morphine given systemically. In contrast no potentiation was obtained with any of the two routes of administration of citalopram when morphine was injected subarachnoidally. The results support the suggested importance of 5-HT terminals in mediation of the supraspinal but not the spinal contribution to morphine antinociception.
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Larsen et al. (1982) studied this question.
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