Author Topic: Blockade and reversal of 5-Methoxy-N, N-Dimethyltryptamine-induced analgesia...  (Read 321 times)

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Archer T, Minor BG, Post C, 1985, 'Blockade and reversal of 5-Methoxy-N, N-Dimethyltryptamine-induced analgesia following noradrenaline depletion', Brain Research, vol. 333, no. 1, pp. 55-61,


 The acute effects of the 5-hydroxytryptamine agonist, 5-Methoxy-N, N-dimethyltryptamine (5-MeO-DMT), upon pain sensitivity, using shock titration, tail-flick and hot-plate methods, in noradrenaline- and 5-hydroxytryptamine-depleted rats were examined. Noradrenaline depletion, following the systemic administration of N-2-chloroethyl-N-ethyl-2-bromobenzylamine hydrochloride (DSP4, 2 × 50 mg/kg, i.p.), caused a reversal of the analgesic effect of 5-MeO-DMT on shock-titration from hypo- to hypersensitivity, and a total blockade of the antinociceptive effect of 5-MeO-DMT upon pain responses in the hot-plate and tail-flick tests. Pretreatment with eitherp-chloroamphetamine (2 × 10 mg/kg) orp-chlorophenylalanine (200, 100, 100 mg/kg), that depletes central 5-hydroxytryptamine stores, failed to alter the analgesia caused by acute 5-MeO-DMT. Strong evidence is provided for the effect of central noradrenaline depletion upon the analgesic effect of the 5-HT agonist. These findings suggest an important tonic influence of the noradrenaline system upon the descending spinal 5-HT pathway in rats.