(+)-8-OH-DPAT and 5-MeODMT induced analgesia is antagonised by noradrenaline depletion.
Physiology & behavior January 1, 1987 T Archer, E Arweström, B G Minor et al. 32 citations
In rats and mice, two drugs that activate serotonin receptors (8-OH-DPAT and 5-MeODMT) reliably produced pain relief in three different tests (tail-flick, hot-plate, and shock-titration). However, when the animals were pretreated with a toxin that destroys noradrenaline neurons (DSP4) given systemically, or with 6-hydroxydopamine injected directly into the spinal cord, the pain-relieving effects of both drugs were eliminated. In the tail-flick test, 8-OH-DPAT actually caused increased pain sensitivity after spinal cord noradrenaline depletion. Biochemical measurements confirmed that the toxins severely reduced noradrenaline in the spinal cord. The findings suggest that the pain relief from these serotonin drugs depends on intact noradrenaline nerve endings in the spinal cord, pointing to a critical interaction between noradrenaline and serotonin systems in spinal pain processing.