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M L Persson

2 papers in the library · 39 citations · publishing 1987-1988

Papers

(+)-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.

DOI: 10.1016/0031-9384(87)90350-7 Full text

Intrathecal noradrenaline restores 5-methoxy-N,N-dimethyltryptamine induced antinociception abolished by intrathecal 6-hydroxydopamine.

Journal of neural transmission January 1, 1988 B G Minor, M L Persson, C Post et al. 7 citations

In rats, destroying spinal norepinephrine (NA) neurons with 6-hydroxydopamine eliminated the pain-relieving effect of the serotonin receptor agonist 5-MeODMT in three different pain tests. Replacing NA directly into the spinal cord restored the analgesic effect. Chemical analysis confirmed a 95% loss of NA in the spinal cord. Destroying serotonin neurons with 5,7-DHT reduced the analgesic effect in one test. The findings show that NA is necessary for 5-MeODMT to produce analgesia and further clarify how NA modulates serotonin-related pain relief.

DOI: 10.1007/BF01250234 Full text