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8-oh-dpat

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BristolRob

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Feb 3, 2006
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Does anyone know whether 8-OH-DPAT has ever been taken by humans?

As a full 5-HT1A agonist, I'm interested whether it would have any behavioural effects. It shuts off the raphe and increases prefrontal DA levels in rats.. I wonder whether it has any hallucinogenic properties for humans in enough concentrations.

If not, then 5-HT2A agonism, 5-HT1A agonism/raphe shut off, decreased tonic 5-HT in hippocampal regions, and perhaps DA burst firing and/or ACh burst firing in medial temporal regions may underly some of LSD's characteristic behavioural effects and be part of an inter-related mode that has similarities with REM sleep, acute psychotic states, temporal lobe epilepsy and related phenomena which may be perceived as slips of the unconscious mind (e.g., deja vu, regressions, relivings, hallucinations, epiphany exerperiences, religious rapture etc)...
 
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Now I can't remember for the life of me where I read this, but I recall reading a study recently, where 5HT1a agonists actually decreased the subjective activity/intensity of 5HT2a-based psychedelics.
 
 
nuke said:
Bump, I'm curious as to if anyone has tried this, I doubt it's psychedelic but I'm very curious as to any other psychopharmacological effect. It releases oxytocin but not vasopressin, which is intriguing.

http://www.ncbi.nlm.nih.gov/entrez/..._uids=12588512&query_hl=5&itool=pubmed_docsum
Click to expand...

I'm also very interested in 8-OH-DPAT. I've read that 8-OH-DPAT produced similar socializing results in rats to that of MDMA. Does anyone know if it can actually be acquired?



Here's another interesting 5-ht-1a agonist that is a strong analgesic, (3-chloro-4-fluoro-phenyl)-[4-fluoro-4-{[(5-methyl-pyridin-2-ylmethyl)-amino]methyl}piperidin-1-yl]methanone, fumaric acid salt:

We report the discovery of F 13640 and evidence suggesting this agent to produce powerful, broad-spectrum analgesia by novel molecular and neuroadaptative mechanisms. F 13640 stimulates G(alphaomicron) protein coupling to 5-HT(1A) receptors to an extent unprecedented by selective, non-native 5-HT(1A) ligands. Fifteen minutes after its injection in normal rats, F 13640 (0.01-2.5 mg/kg) decreases the vocalization threshold to paw pressure; 15 min upon injection in rats that are exposed to formalin-induced tonic nociception, F 13640 inhibits pain behavior. The initial hyperalgesia induced by 0.63 mg/kg F 13640 was followed, 8 hrs later, by paradoxical hypo-algesia; 5 mg/kg of morphine produces the opposite effects (i.e., hypo-algesia followed by hyper-algesia). Repeated F 13640 injections cause an increase in the basal vocalization threshold and a reduction of F 13640-produced hyperalgesia; in these conditions, morphine causes basal hyperalgesia and antinociceptive tolerance. Continuous two-week infusion of F 13640 (0.63 mg/day) exerts little effect on the threshold in normal rats, but markedly reduces analgesic self-administration in arthritic rats. F 13640 infusion also decreases allodynic responses to tactile and thermal stimulations in rats sustaining spinal cord or sciatic nerve injury. In these models of chronic nociceptive and neuropathic pain, the analgesia afforded by F 13640 consistently surpasses that of morphine (5 mg/day), imipramine (2.5 mg/day), ketamine (20 mg/day) and gabapentin (10 mg/day). Very-high-efficacy 5-HT(1A) receptor activation constitutes a novel mechanism of central analgesia that grows rather than decays with chronicity, that is amplified by nociceptive stimulation, and that may uniquely relieve persistent nociceptive and neuropathic pains.

Also, a drug company is currently in phase III trials of a full 5-ht-1a agonist for treatment of depression and anxiety.
 
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Shutting off serotonin sounds kind of scary, are these compounds anxiogenic?

FWIW, I remember that some paper said that some agonists bind to 5-HT1a autoreceptors and others bind to postsynaptic 5-HT1a receptors, but I don't really know
 
I doubt it if it promotes the release of oxytocin and causes sociability similar to MDMA. It's not shutting off serotonin, just one subtype of serotonin receptor
 
Ham-milton said:
I doubt it if it promotes the release of oxytocin and causes sociability similar to MDMA. It's not shutting off serotonin, just one subtype of serotonin receptor
Click to expand...

It promotes sociability similar to MDMA in rats.

Total social interaction:
Without 8-OH-DPAT 119.0(+/-)13.9
With 8-OH-DPAT 207.2(+/-)26.0

Without MDMA 108.2(+/-)3.2
With MDMA 194.5(+/-)11.4
 
Pindolol (a 5HT1a agonist) potentiates DMT in humans according to Strassman, et al.

Why wouldn't 8-oh-dpat do the same?

Strassman said:
We have completed our pindolol study, which was intended to block one of the serotonin receptors believed important in mediating DMT's effects, the serotonin-1A subtype. We have analyzed HRS, blood pressure, and heart rate data, and will soon begin analyzing temperature, ACTH and prolcatin responses. Interestingly, pindolol, discovered by Hofmann at Sandoz, is a lysergaminde derivative, like LSD. It is a small world. Three of the six HRS factors' responses to DMT were enhanced by pindolol, while another two showed strong trends toward enhanced responses. One was unaffected. Blood pressure responses diminished. Thus, it appears, at least for subjective effects, that the 5-HT-1A receptor has a "buffering" effect on DMT, and when this buffering is blocked, psychological and blood pressure responses are more robust. We have begun magnetic resonance spectroscopy (MRS) studies of DMT's effects, having studied three volunteers at fully psychedelic doses, but have failed to see much in the visual cortex, where we assumed most activity would reside. However, these negative results are being used to help justify upgrading our scanning center's hardware and software to allow a newer, more sophisticated method of scanning.
Click to expand...
 
samadhi_smiles said:
Pindolol (a 5HT1a agonist) potentiates DMT in humans according to Strassman, et al.

Why wouldn't 8-oh-dpat do the same?
Click to expand...

I imagine it would. Thought I read somewhere about 5HT1A agonists potentiating psychedelics in general. There was reference to MDMAs potentiating of LSD due to its action on 5-HT1A.
 
Broshious said:
I imagine it would. Thought I read somewhere about 5HT1A agonists potentiating psychedelics in general. There was reference to MDMAs potentiating of LSD due to its action on 5-HT1A.
Click to expand...

i think you mean 5-HT1A antagonist instead of agonist.

This Paper says that pindolol is a weak partial agonist with about 20% efficiency. in the spirit molecule strassman states that we wanted to antagonise 5-HT1A receptors with pindolol. so 8-HO-DPAT should reduce effects of psychedelics (if the potentiation with pindolol wasn't due to activation of 5-HT1A receptors at sites with especially low serotonin concentrations).

sorry for the necrophilia, but i think the 8-OH-DPAT deserves to go up again ;)

any new infos on 8-OH-DPAT? still no human trials?
 
There was a user posting here many moons ago who, if I remember right, took 2-AT to the hundreds of mg's orally (less did nothing) and experienced very negative physical side effects such as hypotensive crisis and unconsciousness. Their advice was to disregard what the rats had said, because it was most certainly different in humans.
 
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