• Psychedelic Drugs Welcome Guest
    View threads about
    Posting RulesBluelight Rules
    PD's Best Threads Index
    Social ThreadSupport Bluelight
    Psychedelic Beginner's FAQ

Tryptamines Benzofuran analogues of Tryptamines (e.g. 5-MeO-BFE)

"I mean, so what if there's some caffeine in a product"

Well,because that means the identity of a substance is BEING MISREPRESENTED.

This is completely unethical, prevent genuine research, and is actually very dangerous - if you establish what you think is a dose-effect profile for a substance, only to later find out it was only 25% pure with the other 75% (to take some arbitrary figures) when someone takes some of 100% pure (and consequently doses 3 times higher than intended), this is clearly not very good, yeah?
Misrepresenting one substance for another(s) entirely is a far larger problem,and today is quite widespread, especially so in the UK RC scene (which is a real travesty - people will seemingly eat or even shoot up almost any unsavoury-looking substances).
 
yer but that's recreational users/addicts full stop we dnt think about this stuff just pop it and see
 
Getting caffeine in your product is the least of your worries playing that game. It's a slippery slope, I'd say there is a spectrum - on one hand you can get purified products with real traceable CoAs with it (probably wont be cheap no), and at the other end of the spectrum there are shops that are selling something by brand names that leave the rest to the imagination, CrazyGnome batch 4 or what the fuck. And you are telling me that is okay? It's literally a crapshoot, basically you are open to someone else deciding for you what you put in your body and you do not even know what it is. Or you think you know what it is but it's actually something else.
There are really a LOT of dirty stimulants out there meaning they are jittery, they fuck with the peripheral nervous system and produce more side- or after effects than the main effects are worth. Maybe at first you are too blunt to notice but after a while don't be suprised if you feel like you have a couple of bratwursts in your sides instead of kidneys.

Anyway I challenge you to argue it is in line with harm reduction to buy and use brand drugs from shady vendors with known scamming affiliation etc. And this is a harm reduction board. So while I appreciate the libertarianism - in the end it's everyone's own decision what they do - that doesn't mean that responsible practice is not very relevant here, it IS. I guess that means you don't have to apologize to anyone but yourself. I know I have been more careless in the past with RC trials (though I knew exactly what they were, there only was relatively little data), and I corrected that mistake.

I'm thankful for datapoints but I don't want to promote a sense of heroism, if you have to prove something to yourself (I guess I had to in the past and sometimes still do, I admit it) that's your own problem... but when bravery is misplaced and risks are being taken recklessly, that can amount to some kind of peer pressure.

What is said to be stupid is not a personal attack, it clearly refers to one of the unwritten rules of proper RC assays: reserve drug combinations for when you have a good body of knowledge to go on. If you have little experence with a known drug, thats unwise, if there is in general very little known about a drug and you want to combine it, that calls for a superlative.

Just be careful guys.
 
yer but that's recreational users/addicts full stop we dnt think about this stuff just pop it and see
The entire aim of Bluelight is to try to dispel that kind of attitude.
What is said to be stupid is not a personal attack, it clearly refers to one of the unwritten rules of proper RC assays: reserve drug combinations for when you have a good body of knowledge to go on. If you have little experence with a known drug, thats unwise, if there is in general very little known about a drug and you want to combine it, that calls for a superlative.

Just be careful guys.
All of this is true. fool's gold, I didn't mean to be rude, I'm sorry, but it comes from a place of love- you could really harm yourself, and I would hate for that to happen. Take care of yourself <3
 
no i know you weren't being rude that's why i pm you first , and the bit about that's just users for you i was just making a point about why i came to this site as this is how we are the truth is 99% of drug users don't use sites like this or really even care what the long term out comes could be , thank god i found this place i now know that after finding out why my muscles where twitching i.e. serotonin syndrome iv been alot closer to offing myself by accident than i ever have before and now know why and which rc do this to me
 
I don't think this compound can give you serotonin syndrome unless it is also an extremely potent serotonin reuptake inhibitor, or you are really, really overdosing it. An even less likely option is that it is somehow undegradeable because of the benzofuran group, and also cannot be transported by the serotonin transporter to help aid processing. But... most things are not impossible so...

Anyways from the 1992 Nichols publication: Benzofuran Bioisosteres of Hallucinogenic Tryptamines

The measured affinities of 3 and 4 for the 5-HT2 receptor labeled by [1251]DOIw ere 95.0 +/- 8.1 and 27.1 +/- 3.5 nM, respectively.

The measured affinities of 2-4 and (f)-a-methyl-B methoxytryptamine for the 5-HT1A receptor labeled by [3H]-8-OH-DPAT were 69 +/- 8.1, 101 +/- 9.5, 779 +/- 63, and 445 +/- 68 nM, respectively.

3: "1-oxa-5-MeO-DMT" or "1-oxa-6-MeO-DMT" ... I believe because 1 is designated to oxa, this forces the MeO to be the 6th position. But this may change the naming on tryptamine because the ethylenedimethylamine group is now at the 2 position, and this needs to be designated. So I think the name is still a bit different but I'm not sure exactly what.

Something like 2-ethylenedimethylamine-6-methoxy-benzofuran? Where the oxygen atom in benzofuran is designated as the 1 position.

4: This one would also have a weird name... my guess is: 2-(methyl,amino)-ethylenebenzofuran or (methyl,amino)-2-ethylenebenzofuran. Haha, this one would give undergrad organic 2 students nightmares!

Anyways so 3, the compound the thread is about, is slightly biased toward 5HT1A. 5HT1A... is most likely a good receptor, but selective or better yet partially selective compounds that share affinity for other well-known psychedelic receptors are to my knowledge not really available. Unless you get lucky and some psiolcybin makes one for you...

Frankly 3 looks interesting as hell and I want to try it!!!!!

! ! !
 
Last edited:
no sorry you got that bit wrong i did not mean this stuff i was just mean how i found out about because of this site its one of these bath salts that did it to me
 
Ahh haha ok. I think it sounds like it could be a very nice compound then.

I think I messed up the naming too. I wasn't understanding the oxa part, but the question is are you still supposed to call it a tryptamine... because it is no longer a tryptamine I think? Sure it is a derivative, but what is the requirement to be called a tryptamine? If Nitrogen in the 5 member ring is, then it is not 1-oxa-MeO-DMT. It has to be a benzofuran...

Instead I think it would be 5-methoxy-7-ethylene(N,N-dimethyl)amine-benzofuran. Or maybe just ethyl instead of ethylene?
 
i lifted this info from the website i got my goo from

IUPAC: [2-(5-methoxy-1-benzofuran-3-yl)ethyl]dimethylamine
Smiles: COC1=CC=C2OC=C(CCN(C)C)C2=C1
InChI: InChI=1S/C13H17NO2/c1-14(2)7-6-10-9-16-13-5-4-11(15-3)8-12(10)13/h4-5,8-9H,6-7H2,1-3H3
Formula: C13H17NO2
Isotope formula: C13H17NO2
Composition: C (71.21%), H (7.81%), N (6.39%), O (14.59%)
Isotope composition: C (71.21%), H (7.81%), N (6.39%), O (14.59%)
Mass: 219.2796
Exact mass: 219.125928793

as a non-chemist it is pretty meaningless to me, but can anyone more learned divine anything useful from it?
 
I stuck in some noparse tags for you to get rid of all the sunglass-wearing smilies. All that says is what the chemical is composed of, but we already knew that.
 
3: "1-oxa-5-MeO-DMT" or "1-oxa-6-MeO-DMT" ... I believe because 1 is designated to oxa, this forces the MeO to be the 6th position. But this may change the naming on tryptamine because the ethylenedimethylamine group is now at the 2 position, and this needs to be designated. So I think the name is still a bit different but I'm not sure exactly what.

No, the carbon that is shared by the phenyl and furan(yl) ring is not counted because it is always saturated, at least as long as the phenyl is unsaturated. Just as with 5-MeO-DMT, the counting is like this:

29ymnx3.png


Something like 2-ethylenedimethylamine-6-methoxy-benzofuran? Where the oxygen atom in benzofuran is designated as the 1 position.

4: This one would also have a weird name... my guess is: 2-(methyl,amino)-ethylenebenzofuran or (methyl,amino)-2-ethylenebenzofuran. Haha, this one would give undergrad organic 2 students nightmares!

You do know that the IUPAC name is mentioned twice on the wiki page? It's 2-(5-methoxy-1-benzofuran-3-yl)-N,N-dimethylethanamine.

Another name for 5-MeO-DMT is 5-methoxy-3-[2-(dimethylamino)ethyl]indole, since the indole nucleus is replaced by a benzofuran nucleus you would simply get 5-methoxy-3-[2-(dimethylamino)ethyl]benzofuran.

Oops sorry you were talking about compound 4 - which is a bit confusing to people who do not have the article, and apparently to me as well.

Well compound 4 is this one, the benzofuran analogue of 5-MeO-AMT:

199hxt.png


I don't know why it interests you? 5-MeO-AMT sounds like one of the vilest psychedelics out there.

Anyways so 3, the compound the thread is about, is slightly biased toward 5HT1A. 5HT1A... is most likely a good receptor, but selective or better yet partially selective compounds that share affinity for other well-known psychedelic receptors are to my knowledge not really available. Unless you get lucky and some psiolcybin makes one for you...

Frankly 3 looks interesting as hell and I want to try it!!!!!

! ! !

OK well first I was untrusting of 5-HT1A agonism (or higher relative affinity for it) was that good of an idea since if you check the list of brain functions associated with it and the effects 5-MeO-DMT can have it probably isn't doing very positive things for it. But perhaps that is not true, DMT can be anxiolytic and has 5-HT1A affinity, perhaps its delicate and can produce uncomfortable side-effects as well - panic maybe? Or are there primarily positive things to be expected from 5-HT1A activity?
Alpha,N,N-TMT is said to be similar to aMT, only less potent - I wonder about that one, if it's worth it... aMT itself is very trancey and lethargic to me, I wonder if 5-HT1A activity is involved.

Curious about this one:

t0rgix.png


Also I am not sure if we should just rename this thread to "benzofuran analogues of tryptamines" (the word bioisostere probably does not help anyone ;) )
 
Great post Solipsis! I think we all needed a little clarification on the structures we have been discussing here. I think it might be a good idea to rename this thread as you suggested. However, how many of these benzofuran analogues are even suspected to be active? Does the replacement of the indole nitrogen with oxygen really not have that much of an effect on receptor binding, etc?
 
Oh I see about the naming. That is a dirty little trick to skip the unsaturated carbon. Anyways I don't think you can call them tryptamine analogs because it doesn't have the indole. It has benzofuran, so I think it should be "Dimethylethanamine analogs of benzofuran."

Or maybe 5-MeO-DMEB or 5-MeO-DMEBZF even.

Indole yes both of the compounds "3 and 4" have good activity at both 5HT1A and 5HT2 (I assume 2A but the paper from 1994 just says 2), with 3, the subject of the thread showing the most interesting profile. This is all the particular paper characterizes though (see my previous post for the information).

Anyways back to the real matter, 5HT1A. So I have suspected for a while that 5HT1A is important for driving a lot of the sexual response psychedelics elicit. Here is some data from a few papers:

Receptor profiling from "Psychedelics and the human receptorome"

5ht1a: 4.00 5-MeO-MIPT, 4.00 lisuride, 4.00 DOET, 4.00 SS-
2c, 4.00 5-MeO-DIPT, 4.00 DIPT, 4.00 5-MeO-DMT, 4.00 cis-
2a, 4.00 DPT, 3.73 LSD, 3.61 mescaline, 3.59 RR-2b, 3.48 5-
MeO-TMT, 3.45 TMA, 2.97 EMDT, 2.91 2C-E, 2.88 psilocin,
2.81 6-F-DMT, 2.75 2C-B, 2.38 MDA, 2.31 DOI, 2.20 2C-T-2,
2.04 4C-T-2, 1.79 2C-B-fly, 1.51 DOM, 1.18 DOB, 0.98 Aleph-2;
0.00: TMA-2, MEM, MDMA, DMT, ibogaine, salvinorin A;
ND: morphine, THC

Note how the MiPT and DiPT compounds are at the top for this one. I'm not sure if you have seen this paper before, but it is a PLoS One publication and can be found for free just look up the title.

4-AcO-DiPT is pretty strong at sex drive stimulation too, but they didn't test it. At the top of this list I have only tried LSD and at very low ineffective does 5-MeO-DMT. I think 5-MeO-DMT, from what I have read, is not suited for this use though heh.

Another paper about 5HT1A and MDMA:

Neurochem Int. 2007 Dec;51(8):496-506.
Short-term effects of 3,4-methylen-dioxy-metamphetamine (MDMA) on 5-HT(1A) receptors in the rat hippocampus.
Giannaccini G, Betti L, Pirone A, Palego L, Fabiani O, Fabbrini L, Mascia G, Giusti L, Macchia M, Giusiani M, Martini C, Lucacchini A.
Source

Department of Psychiatry, Neurobiology, Pharmacology and Biotechnology, University of Pisa, Via Bonanno 6, Pisa 56126, Italy.
Abstract

The first effects of 3,4-methylen-dioxy-metamphetamine (MDMA, "ecstasy"), on serotonin 1A (5-HT(1A)) receptors in rat hippocampus were determined by means of [(3)H]-8-hydroxy-dipropylamino-tetralin ([(3)H]-8-OH-DPAT) and 5'guanosine-(gamma-[(35)S]-thio)triphosphate ([(35)S]-GTPgammaS) binding as well as inhibition of forskolin (FK)-stimulated adenylyl cyclase (AC) activity. The study was completed by [(35)S]-GTPgammaS functional autoradiography experiments carried out in frontal sections of rat brain, including the hippocampal region. Results showed that MDMA was either able to displace [(3)H]-8-OH-DPAT binding (K(i) congruent with 500 nM) or to reduce the number of specific sites (B(max)) without affecting K(d). The drug also failed to change the [(35)S]-GTPgammaS binding or to inhibit AC velocity, underlying its behavior as a non-competitive 5-HT(1A) receptor antagonist. Further, MDMA (1 or 100 microM), partially antagonized either [(35)S]-GTPgammaS binding stimulation of the agonists 5CT and 8-OH-DPAT or the AC inhibition induced by 5CT and DP-5CT. However, in contrast to binding studies, in AC assays the amphetamine displayed an effect also on EC(50), always being less potent than the reference antagonist WAY100,635. In functional autoradiography, MDMA behaved either as a partial 5-HT(1A) antagonist in limbic areas or, added alone, as an agonist, increasing the coupling signal presumably through 5-HT release from synapses. Interestingly, the selective 5-HT re-uptake inhibitor (SSRI) fluoxetine had no effect on MDMA [(35)S]-GTPgammaS binding activation. This latter finding indicates that the amphetamine can release 5-HT via alternative mechanisms to 5-HT transporter binding, probably via membrane synaptic receptors or vesicular transporters. The release of other transmitters is not excluded. Therefore, our results encourage at extending the study of MDMA biochemical profiles, in the attempt to elucidate those amphetamine-induced pathways with a potential for neurotoxicity or psycho-stimulant activity.

From the concluding paragraph of the previous paper, because their abstract is quite confusing!

The present work provides new data describing a direct role
for hippocampal 5-HT1A receptors in MDMA mechanisms of
action: the drug intrinsic activity on 5-HT1A receptors is
consistent to that of a partial antagonist in this area. The
compound attenuates 5-HT1A receptor density and its coupling
to G proteins as well as, with lower effectiveness, its inhibitory
response on AC activity in the rat hippocampus.In in vivo-like
conditions, MDMA displays the activity of both an agonist or
antagonist
, following a region-dependent profile.

It's probably just an agonist... their ways of testing things could be too complicated I am guessing. Bottom line is they show a clear link between MDMA and 5HT1A. It is hard to see how this could be anything but agonism caused by serotonin release. The antagonism could just be an assay artifact, or their weird assays show some incorrect results.

There's not much else I have been able to find, there really isn't much work in the area. But I think what little there is looks pretty promising, really we just need a drug that hits 5HT1A with good potency and not too much else to get a good idea of what it is capable of... anything recreationally useful or not.

I would be interested to hear a bit more about 5-MeO-DMT though. It seems most people think it is too deranging to be really useful. I wonder if perhaps this is related to activity at other receptors? The receptorome paper has some data on it:

5-MeO-DMT: 4.00 5ht1a, 3.69 5ht7, 3.48 5ht1d, 2.73 5ht6,
2.41 5ht1b, 2.38 D1, 1.84 5ht5a, 1.72 5ht1e, 1.58 D3, 1.57
Alpha2C, 1.55 5ht2c, 1.00 Alpha2A, 0.98 5ht2a, 0.97 SERT,
0.88 Imidazoline1, 0.86 Alpha2B, 0.82 NET, 0.78 D4, 0.73 D2,
0.69 5ht2b; 0.00: Alpha1B, Beta2, Beta1, DAT, D5, Alpha1A,
Sigma1, Sigma2, CB2, KOR, Ca+Channel, M1, M2, M3, M4,
M5, H2, CB1; ND: H1, DOR, MOR, NMDA

Where they show it has the most relative potency at 5HT1A, but then has a lot of activity at 5HT7 and 5HT6. I forget exactly how they get the 4.0 value, it could be more potent at the other receptors per molecule, but relative to standard it is most potent at 5HT1A. Regardless it has a very broad activity range, if you get the paper it is pretty high up on the breadth list. I would have to guess 5-MeO-DMT is not suited for determining what uses 5HT1A agonism has.

We had been discussing on another forum that these receptor probably are not very recreational. 5HT1D and 1B I believe we crossed off the list as well... so it is hard to say at this point...
 
Last edited:
Oh I see about the naming. That is a dirty little trick to skip the unsaturated carbon. Anyways I don't think you can call them tryptamine analogs because it doesn't have the indole. It has benzofuran, so I think it should be "Dimethylethanamine analogs of benzofuran.

An analogue means that a compound is similar but different in a certain aspect. We certainly could call this thread "Benzofuran analogues of tryptamines" and the term benzofuran analogue would refer to: an analogue of tryptamine that is a benzofuran. Implicit in that is that this benzofuran is similar to tryptamine but it is not one, so the absence of the indole or whole tryptamine nucleus does not matter. I will rename the thread in a minute.
And a homologue indicates some discrete repetition of analogy like the extension of the 4-pos. moiety of 2C-D to 2C-E and further to 2C-P.

Or maybe 5-MeO-DMEB or 5-MeO-DMEBZF even.

You know, dimemebfe is short for dimethyl methoxy benzofuran ethanamine right? But look at DMT and 5-MeO-DMT, the N,N-dimethyl is absent in the trivial name DMT and also absent in 5-MeO-DMT. You will rarely see 5-MeO-N,N-DMT written somewhere even if that is right. So, if we need an acronym we can just take the BFE for benzofuran ethanamine. It replaces the T of tryptamine, so that dimemebfe becomes 5-MeO-BFE. The non 5-MeO version does not even seem to be a topic of discussion but it could be called DMBFE or N,N-DMBFE. Shall we baptize and rename to 5-MeO-BFE?

Indole yes both of the compounds "3 and 4" have good activity at both 5HT1A and 5HT2 (I assume 2A but the paper from 1994 just says 2), with 3, the subject of the thread showing the most interesting profile. This is all the particular paper characterizes though (see my previous post for the information).

Anyways back to the real matter, 5HT1A. So I have suspected for a while that 5HT1A is important for driving a lot of the sexual response psychedelics elicit. Here is some data from a few papers:

5ht1a receptor profiling
0.00: TMA-2, MEM, MDMA, DMT, ibogaine, salvinorin A;
ND: morphine, THC

0.00? How is that even possible, it's not nM I presume because that would mean that it would displace a ligand competing for the receptor (half of them?) at a concentration of zero?

Note how the MiPT and DiPT compounds are at the top for this one.

Am I blind or are they not listed? edit: okay I was blind about the DiPT but I only see the 5-MeO analogue of MiPT.

I'm not sure if you have seen this paper before, but it is a PLoS One publication and can be found for free just look up the title.

4-AcO-DiPT is pretty strong at sex drive stimulation too, but they didn't test it. At the top of this list I have only tried LSD and at very low ineffective does 5-MeO-DMT. I think 5-MeO-DMT, from what I have read, is not suited for this use though heh.

Another paper about 5HT1A and MDMA:





It's probably just an agonist... their ways of testing things could be too complicated I am guessing. Bottom line is they show a clear link between MDMA and 5HT1A. It is hard to see how this could be anything but agonism caused by serotonin release. The antagonism could just be an assay artifact, or their weird assays show some incorrect results.

Acting as both an agonist as well as antagonist? That just means partial agonist right? Or perhaps the difference is that a partial agonist can be both but dose or concentration dependent whereas an agonist+antagonist may indicate that it depends on a certain biochemical state of the receptor. I assume it's not about different subtypes (1A already is one and they cloned it right?) so I agree if its not a partial agonist it is confusing. Not sure to do with the info in that case.

There's not much else I have been able to find, there really isn't much work in the area. But I think what little there is looks pretty promising, really we just need a drug that hits 5HT1A with good potency and not too much else to get a good idea of what it is capable of... anything recreationally useful or not.

I would be interested to hear a bit more about 5-MeO-DMT though. It seems most people think it is too deranging to be really useful. I wonder if perhaps this is related to activity at other receptors? The receptorome paper has some data on it:

[/quote]

Maybe sigma activity? I personally don't really understand the reason why 5-MeO-DMT is as hardcore and profound. Maybe it has some special way of activating signaling pathways or cascades in particular parts of the brain like the temporal or frontal lobe? Of course when snorted or smoked what also matters is how it surprises or rushes the BBB and that may disable the body's ability to anticipate the effect. It is quite astonishing how the body and brain are able to activate countermeasures from the mental anticipation of taking a drug. The reason why setting-based tolerance exists has to be related to this. The same fact that DMT is metabolized very quickly may be connected to the fact that it is relatively hard to get DMT tolerance and why it is so intense: because it has a sort of 'flooding' effect. I would expect oral DMT with a MAOI to produce tolerance like most other psychedelics. Can anyone confirm this?

Where they show it has the most relative potency at 5HT1A, but then has a lot of activity at 5HT7 and 5HT6. I forget exactly how they get the 4.0 value, it could be more potent at the other receptors per molecule, but relative to standard it is most potent at 5HT1A. Regardless it has a very broad activity range, if you get the paper it is pretty high up on the breadth list. I would have to guess 5-MeO-DMT is not suited for determining what uses 5HT1A agonism has.

We had been discussing on another forum that these receptor probably are not very recreational. 5HT1D and 1B I believe we crossed off the list as well... so it is hard to say at this point...

Ahhh well that answers my previous question about the values.

Though it says that 5-MeO-MiPT has a value of 4 at the top, for 5-HT1A... well I find that particular compound to be the most stimulating tryptamine of all that I have tried, so this again makes me suspicious about the whole thing. Then again I never heard about N,N-DiPT causing anxiety. It seems to me like it's way more complex than we are trying to make it. Unfortunate that we have a hard time pinning 5-HT1A down as much as 5-HT2 seems to be pinned to psychedelia.

I'd be interesting to find a dedicated thread in ADD where the info of the role of different 5-HT receptor subtypes are explained by people who know their stuff.
 
Last edited:
0.00? How is that even possible, it's not nM I presume because that would mean that it would displace a ligand competing for the receptor (half of them?) at a concentration of zero?

Soli, those are weighted Ki values (not logKi or anything) where 0= no binding and 4 = strong binding, ND = no data. It's a crap scheme but it's what the paper uses for ranking them. There's an XLS with real Ki values if you'd prefer.
 
I am not sure there is anything discussing all the 5HT subtypes together really.

I believe the primary key to having a good psychedelic is the ability to hit multiple receptors simultaneously. The reason drugs like DMT and LSD are so effective... they hit more than one receptor at the same time, thus stimulating many pathways all at once. If you go through the Receptorome paper you will get a feel for just how promiscuous good psychedelics really are.

The question though is which ones do you really need, and which ones do you not? I should post part of the discussions we had on another forum around this. There are some 5HTRs that seem to be pretty much junk, probably responsible for a lot of the GI discomfort or other undesirable effects and less of the desirable mental aspects.

But they are probably not inseparable entirely. Pure 5HT2A agonists are probably pretty limited for instance. As far as I know the closest thing to a pure 5HT2A agonist comes from the NBOMe series, but I thought even these are expected to have activity at other 5HTRs, even if it is just "a little" or "some?"

Anyways you were wondering about the MDMA study, yeah like I said the assays they use are pretty quirky. I haven't read the paper is extremely great detail, but this is required to understand exactly what they were doing, that coming from me who has a very good grasp and lots of experience with in vitro assays and GPCRs. They do some non-standard stuff, using multiple ligands simultaneously to get the antagonist result.

Personally I think they probably overdid it and got some "they're true but not really because we did too much manipulation" type results.

LOL and regarding the name... I think to be 100% correct you really have to include the dimethyl... DMT and 5-MeO-DMT are not just "T" and "5-MeO-T" for a reason right? ... so my final vote is for 5-MeO-BFDME. =P
 
Shit I totally forgot about this! The main reason I am interested in 5HT1A... the purported link to oxytocin! LOL, here were a few more papers including a new one I just found:

The original one I forgot about first...

Neuroscience. 2007 May 11;146(2):509-14.
A role for oxytocin and 5-HT(1A) receptors in the prosocial effects of 3,4 methylenedioxymethamphetamine ("ecstasy").
Thompson MR, Callaghan PD, Hunt GE, Cornish JL, McGregor IS.
Source

School of Psychology, University of Sydney, Griffith Taylor Building (A18), Sydney, NSW, 2006, Australia.
Abstract

The drug 3,4 methylenedioxymethamphetamine (MDMA; ecstasy) has a widely documented ability to increase feelings of love and closeness toward others. The present study investigated whether oxytocin, a neuropeptide involved in affiliative behavior, may play a role in this effect. A moderate (5 mg/kg, i.p.) dose of MDMA increased social interaction in male Wistar rats, primarily by increasing the amount of time rats spent lying adjacent to each other. MDMA (5 mg/kg) activated oxytocin-containing neurons in the supraoptic and paraventricular nuclei of the hypothalamus, as shown by Fos immunohistochemistry. MDMA (5 mg/kg i.p.) also increased plasma oxytocin levels and this effect was prevented by pre-treatment with the 5-HT(1A) antagonist N-[2-[4-(2-methyoxyphenyl)-1-piperazinyl]ethyl]-N-2-pyridinylcyclohexanecarboxamide maleate salt (WAY 100,635; 1 mg/kg i.p.). The oxytocin receptor antagonist tocinoic acid (20 microg, i.c.v.) had no effect on social behavior when given alone but significantly attenuated the facilitation of social interaction produced by MDMA (5 mg/kg). The 5-HT(1A) agonist 8-hydroxy-2-(di-n-propylamino)-tetraline) (8-OH-DPAT, 0.25 mg/kg, i.p.) increased social behavior in a similar way to MDMA and this effect was also significantly attenuated by tocinoic acid. Taken together, these results suggest that oxytocin release, stimulated by MDMA through 5-HT(1A) receptors, may play a key role in the prosocial effects of MDMA and underlie some of the reinforcing effects of the drug.

And the new boy...

Brain Res Bull. 2011 Aug 10;86(1-2):65-73.
MDMA-induced c-Fos expression in oxytocin-containing neurons is blocked by pretreatment with the 5-HT-1A receptor antagonist WAY 100635.
Hunt GE, McGregor IS, Cornish JL, Callaghan PD.
Source

Discipline of Psychiatry, Sydney Medical School, University of Sydney, Concord Hospital, NSW, Australia.
Abstract

The popular party drug MDMA (3,4-methylenedioxymethamphetamine, "Ecstasy") increases sociability in both humans and laboratory animals. Recent research suggests that these prosocial effects may involve serotonin (5-HT)-stimulated hypothalamic release of the neuropeptide oxytocin. WAY 100635, a 5-HT(1A) receptor antagonist, prevents MDMA-induced increases in plasma oxytocin and also reduces MDMA-mediated increases in social interaction in rats. The present study used c-Fos immunohistochemistry to determine the possible role of 5-HT(1A) receptors in MDMA-mediated activation of oxytocin synthesizing neurons. Male Wistar rats (n=8/group) were administered MDMA (10 mg/kg, i.p.) with or without WAY 100635 (1 mg/kg, i.p.) pre-treatment and c-Fos expression was then assessed throughout the brain. MDMA significantly increased locomotor activity and this effect was partly prevented by WAY 100635, in agreement with previous studies. WAY 100635 significantly reduced MDMA-induced c-Fos expression in a subset of brain regions examined. A particularly prominent reduction was seen in the oxytocin-positive neurons of the supraoptic nucleus and paraventricular hypothalamus, with more modest reductions in the Islands of Calleja, median preoptic nucleus, somatosensory cortex and nucleus of the solitary tract. WAY 100635 did not alter MDMA-induced c-Fos expression in the striatum, thalamus, or central amygdala. These results indicate that MDMA's action on oxytocin producing cells in the hypothalamus is mediated through 5-HT(1A) receptors and that certain specific cortical, limbic and brainstem sites are also activated by MDMA via these receptors.

:) :) :)
 
Top