(+)-8-OH-DPAT and 5-MeODMT induced analgesia is antagonised by noradrenaline depletion.
T Archer, E Arweström, B G Minor, M L Persson, C Post, E Sundström, G Jonsson
Physiology & Behavior 1987 DOI: 10.1016/0031-9384(87)90350-7 (opens in new tab)
Study at a glance
AI-extracted from the abstract| Characteristics | Experimental study Peer reviewed |
|---|---|
| Population | Rats and mice |
| Interventions | 8-OH-DPAT 5-MeODMT DSP4 6-OHDA |
| Dose | 1 mg/kg SC |
| Citations | 32 |
| Key findings | The analgesic effects of the serotonin agonists 8-OH-DPAT and 5-MeODMT depend on intact spinal noradrenaline terminals, as depleting noradrenaline abolished or reversed pain relief. |
Abstract
In experiments with both rats and mice the 5-HT agonists 8-hydroxy-2-(di-n-propylamino)tetralin (8-OH-DPAT) and 5-methoxy-N,N-dimethyl-tryptamine (5-MeODMT) were shown to produce reliable analgesic effects after acute administration (1 mg/kg SC) in the tail-flick, hot-plate and shock-titration tests of nociception. Prior treatment with the noradrenaline neurotoxin, N-2-chloroethyl-N-ethyl-2-bromobenzylamine (DSP4), systemically administered to both rats and mice abolished the analgesic effects of both the 5-HT agonist compounds in all the tests of nociception used. Intrathecal 6-hydroxydopamine (6-OHDA) treatment also abolished the analgesic effects of 8-OH-DPAT and 5-MeODMT; in the tail-flick test the analgesia induced by 8-OH-DPAT was reversed to an hyperalgesia. Biochemical analyses confirmed notable noradrenaline depletions in the spinal cord. It is concluded that an important interaction between presynaptic noradrenergic terminals and serotonergic receptor sites, possibly 5-HT1A, mediates spinal nociception processes.