Tryptoline Psychedelics?

[TheAzo]

PNU-22394 is an active 5HT2A agonist and is close in structure to beta-carbolines, if not identical. But much higher efficacy at 5HT2C so it would be a weird and creepy psychedelia at best.

http://en.wikipedia.org/wiki/PNU-22394

And also an 5HT2B agonist as well, which is a bad thing.

Do you have info on what 5HT2C agonists do, subjectively?

 

[ebola?]

most of the commentary is people inferring from how mcpp feels.

ebola

 

[N0 W4RN1NG]

Also, most 5HT2C antagonists are effective anxiolytics, so that counts for something.

I've taken syrian rue extracts by themselves and IMHO there is certainly more psychedelia than an ordinary MAOI, like phenelzine, has.

 

[fastandbulbous]

^ Makes sense seeing that I've seen 5HT2c agonists labelled as panicogens

 

[Amberthefrog]

What's a panicogen?

 

[immad]

^Something that induces panic.

 

[zero zero]

MPTP which is the actual dangerous species which makes MPP+ in vivo, theoretically MPP+ cannot hurt even if you inject it unless you get it past the BBB not that I would want to test the theory, and the betacarbolnes are close cousins, if a nitrogen bridge is made between the piperidine and phenyl of MPTP you get a tetrahydrobetacarboline, and yes this betacarboline is an effective DA neurotoxin too. it is this 'derivative' of MPTP that shulgin refers to in the back of Pihkal. there are also some pretty effective isoquinoline neurotoxins which work the same way, by becoming permanently charged inside the the brain so they can't get back out and then they spin out free radicals as the oxidase system tries to chew them up

does B caapi contain tryptamines as well as carbolines? or am I thinking of some other South American plant.

My only harmine experience was with material extracted from Aldricha chimica and it was delerium. perhaps Rue or B caapi are kinder materials though rue contains some other unpleasant alkaloids.

How do you know that it is toxic.

 

[/navarone/]

Wait isn't MPP+ neurotoxic due to the cherged quaternary nitrogen?
B-carboline lacks the methyl group present in MPP+, I dont se how that nitrogen could become methylated in vivo.

 

[Coolio]

^ Makes sense seeing that I've seen 5HT2c agonists labelled as panicogens

Are you sure? Can you find numbers on 5-MeO-DIPT's 5-HT2c agonist effect?

What I just gathered from quick research is that 5-MeO-DIPT and LSD are particularly ineffective at 5-HT2c agonism compared to other psychedelics; and that they're more of a 5-HT2a agonist than a lot of other psychedelics.

LSD and 5-MeO-DIPT are the two psychedelics that I consider panicogens for me.

 

[Hammilton]

What I just gathered from quick research is that 5-MeO-DIPT and LSD are particularly ineffective at 5-HT2c agonism compared to other psychedelics; and that they're more of a 5-HT2a agonist than a lot of other psychedelics.

Well LSD is hugely more potent at 5HT2a, but it's only 20-25% of the efficacy of 5HT, which is quite interesting.

 

[/navarone/]

Hmm...so considering that LSD has a 5 nm 5-HT2a Ki affinity, then 5-HT should have a 0 nm Ki affinity right? (forgive me if this sounds obvious)

 

[Hammilton]

Obvious? it doesn't even make sense. I have no idea what you're asking.

 

[tryp2fun]

Hmm...so considering that LSD has a 5 nm 5-HT2a Ki affinity, then 5-HT should have a 0 nm Ki affinity right? (forgive me if this sounds obvious)

Not at all. The affinity has nothing to do with the efficacy. The affinity is the concentration required to get the response. The efficacy is the response due to the compound compared to the natural ligand. In the case of LSD, the efficacy is much lower than serotonin, 25%, so it is only a partial agonist. All of the psychedelics are partial agonists at 5HT-2a receptors.

 

[Hammilton]

All of the psychedelics are partial agonists at 5HT-2a receptors.

no they're not

 

[/navarone/]

Not at all. The affinity has nothing to do with the efficacy. The affinity is the concentration required to get the response. The efficacy is the response due to the compound compared to the natural ligand. In the case of LSD, the efficacy is much lower than serotonin, 25%, so it is only a partial agonist. All of the psychedelics are partial agonists at 5HT-2a receptors.

Ow..
Thanks, that cleared a lot on confusion. I thought affinity was the likeness of, or 'how well' a ligand to bind to a receptor.

 

[Holy_cow]

Harmaline, injected im in a dose of sereral 100mg is clearly a hallucinogen and does not cause a toxic delerium like the anticholinergics. This is from my personal experience, made some 25 years ago.

they are all B-carbolines. as this is the parent ring structure.
tryptoline is tetrahydrobetacarboline

these don't really seem to be psychedelic on their own though for a while harmine was thought to be psychedelic, In my opinion it is more a wavy vomiting toxic delerium. Some of them are dangerously neurotoxic.

 

[(zonk)]

Ibogaine is almost a b-carboline, anyway ive been wondering about the actual psychedelic activity of endogenous pineal products like pinoline and tryptoline as there pharmalogical and structural simularities to harmala and iboga alkaloids. Ive ordered some but been so busy ive had no time to test. I have 1g samples each of tryptamine and tryptoline along with methylene blue and L-me for biosynthesis of dmt at somepoint. Nothing like endogenous ethneogens

 

[(zonk)]

And harmala does have its own minor psychedelic properties