Abstract
The effects of the 5-hydroxytryptamine type-2 (5-HT 2) receptor agonist (±)-1-(2,5-dimethoxy-4-iodophenyl)-2-aminopropane (DOI) and the 5-HT 1A agonist (+)-8-hydroxy-2-(di- n-propylamino)-tetralin [(+)-8-OH-DPAT] on nociceptive responsiveness were compared in mice. Intrathecal administration of DOI (5–20 μg) produced a dose-dependent behavioural syndrome, consisting of biting or licking, directed towards the caudal part of the body and reciprocal hindlimb scratching. However, (+)-8-OH-DPAT (5–20 μg) did not produce the biting and scratching behaviour. The response to DOI (20 μg) was reversed by treatment with the substance P receptor antagonist, [ d-Arg 1, d-Trp 7,9, Leu 11]-SP (Spantide) (8 μg). The tail-flick reflex was markedly depressed 5–20 min after administration of (+)-8-OH-DPAT; DOI did not change the tail-flick reflex after 5 min but significantly inhibited the reflex response 10–20 min after injection. The data show that stimulation of 5-HT 2 receptors, but not 5-HT 1A receptors, induced a behavioural syndrome, which may reflect activation of nociceptive pathways. The tail-flick reflex was more markedly inhibited by stimulation of 5-HT 1A than 5-HT 2 receptors. Accordingly, 5-HT 2 and 5-HT 1A receptors seem to have a different function in the modulation of nociceptive responsiveness in the mouse.
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