Effect of monoamine transmitters on 3-acetyiaconitine analgesia

The latency of heat-induced tail-flick was prolonged after the rats were given 3-acetylaconitine (AAc) 20-40 vg/kg ip or 0.1-0.5 vg icv. The analgesia of AAc was dose-dependent. The most intense analgesia with AAc was seen at 30-45 min after ip or icv, and followed by a time-dependent decrease in activity. The relative potency of analgesic effect of AAc was 67 (ip) or 10 (icv) times that of morphine. AAc (30 vg/kg, ip) potentiated the analgesia of morphine (5 mg/kg, sc) which was reversed by naloxone (4 vg, icv) but did not affect the analgesia induced by AAc. AAc-induced analgesia was markedly reduced by reserpine, dl-p-chlorophcnylala-nine, p-chloroamphetamine, 6-hydroxydopa-mine. dopamine, apomorphine or selegiline, and enhanced by 5-hydroxytryptamine (5-HT), norepinephrine (NE), cyclic AMP, pargyline or haloperidol. The decrease of the analgesic effect of AAc induced by reserpine was reversed by combined administration of l-tryptophan, 5-HT, l-dopa, NE or a-methyldopa. It is concluded that the analgesic effect mediated by AAc is closely related to responses involving the central catecholaminergic and serotoninergic systems.