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Piribedil

oh my god its a - METHYLENE DIOXY group!!! THATS SO INTERESTING! you know, because its like ECSTASY!!!



do you at least have something to say about it, more than posting a picture and saying its 'interesting' ?
 
If he added "I wonder if its active" it would have been like 50 percent of the posts on here.

I fail to see the difference.
 
Looks like a possible stimulant, though I doubt it's going to be very enjoyable.
edit: now that i've actually read the wiki, it sounds even less enjoyable.
 
Fuck... how can you be so arrogant? It is really an offense to you guys if someone comes here and post another molecule? Are you so knowledgeable like that? I found it interesting because I personally do not know many dopamine agonists with that kind of structure. I'm not looking for bloody MDMA analogs, cristaline MDMA it's pretty good by itself.. And because I'm much more into cognitive enhancement than recreative use of substances.. That was not nice :(
 
Dopamine agonists aren't recreational substances AFAIK.

think DARIs and you'll be better off.

And the reason you got the response you did is because of the work you put into your post. You didn't even bother to have the image viewable in here, we had to go to wiki and look at it. Then all you added was "interesting structure" wow. Why was it an interesting structure? Because you had a benzene hooked to an MD? What sort of response did you expect? The only reason anyone could consider that structure interesting is because there's an MD on a remotely stimulanty-structure.

Hell, all you had to do was UTFSE and you've have found that there was another thread on the subject in 2005 and it was deemed a useless substance.

It's not a stimulant (I was wrong :( )
 
IIRC it's a D2/D3 agonist and alpha2 antagonist (alpha2 are autoreceptors), so it could be somewhat stimulating.

Anyway, what's the final word on the reason that direct DA agonists are not stimulating? A few points I seem to remember from previous discussions:

1. Autoreceptor activation? But why is inhibition of dopamine release so bad if the direct agonist is activating the postsynaptic dudes anyway?

2. Not getting to the right brain region? Could anyone explain how that works, I thought it just diffuses?

3. Different effect on the receptor than dopamine? (Similarly to the story with 5-HT2A)

4. Lack of NA stimulation?

Oh, and biting the greenlighters is not nice (especially when you do it by second guessing their intentions). Welcome, Kolmogorov :)
 
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the post synaptic dudes, lol. That's hilarious.

I don't think they were being harder on the bluelighters than they would have been on anyone else. To test this, I'm gonna search out a MD-containing dopamine agonist and post about it in a month. If I'm ripped to shreds, we'll know. And I don't think we were second guessing anything- when so little thought and effort is put into a post, what did he (I'm assuming, and you know what that does...) expect?

Inhibition of dopamine release is a bad thing because it causes a lot of negatives, ie: horrible nausea. In this case it's a bad thing because of your question #3. Dopamine seems to be the king of dopamine receptor agonists, imho. Nothing does what it does or as well as it does.

4. Is not essential for a good stimulant. There are wonderful stimulants out there with little to no NARI effect

I've done a lot more studying on GABA receptors and GABAergics than I have dopamine, so I may not be batting 1000 here.
 
Of course I did not researched it. I just posted a link. Didn't knew that posting a bloody link would make me get flamed, though.:\ But in retrospect. it was a very stupid thread that's what happen when you don't sleep for 36 hours and don't do drugs meanwhile
 
I got prescribed Piribedil once.
It is not recreational at all.

It comes in 20mg IR pills and 50mg XR pills. I got the 50mg ones.
I tried from 50mg to 300mg.

It did nothing AT ALL, except making me nauseous (like many dopaminergic agonist would do.... Domanine agonists = emetics, like Apomorphine.....)

Quite an useless medication, IMO.
It is prescribed as an antiparkinsonian: there are much better ones.
It's also prescribed for cognition deficit (that's why I got it prescribed, along with Piracetam); there are much better alternatives.
It is also a vasodilator: there are better ones with less side effects.

Crappy, shitty, useless medication.
 
Yup, dopamine agonists are godawful except for maybe LSD.

4. Is not essential for a good stimulant. There are wonderful stimulants out there with little to no NARI effect
Click to expand...

Like which? Everyone here calls MDPV a selective DARI but the data I recall reading on its receptor affinity was 3:1 NET:DAT. If someone has this data and could illuminate the subject, please do! I'm also curious to the dopamine selective stimulants. So far as I can tell highly selective dopaminergic stimulants (like RTI-121) have rarely ever been tasted.

It seems like a rather complicated issue as to the psychopharmacy, you have a lot of people with ADHD displaying decreased amounts of DAT in the nucleus accumbens (more dopamine in the reward center) but a quarter of them exhibiting depression (several fold higher than the rate of the general populace).

The PET scans revealed that ADHD subjects had significantly fewer dopamine transporters than control subjects in the nucleus accumbens, an area of the ventral striatum that is one of the main reward centers in the brain. In a dorsal striatum region known as the putamen, which plays an important role in habits and is also involved with attention, dopamine transporter levels did not differ between the two groups.

In both groups, levels of dopamine transporters in the putamen were positively associated with scores of inattention on the self-report questionnaire: the higher the level of transporters, the higher the score of inattention. This finding makes it clear that dopamine transporters play an important role in modulating attention in all people. Yet, for a given level of dopamine transporters, scores of inattention were, on average, five times greater for ADHD subjects than for controls in this study.
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http://www.bnl.gov/bnlweb/pubaf/pr/PR_display.asp?prID=06-124

Also on ADHD/dopamine:
Genetically engineered “knockout” mice that lack the gene encoding the dopamine transporter (DAT-KO mice) have become available. These mice demonstrate remarkable hyperactivity. This is thought to be due to the greater than 5-fold elevation of extracellular dopamine levels within the striatum, the major motor area of the brain. It is worth mentioning that the knockout mice behave essentially like their normal littermates when placed in a familiar environment. However, when place in a novel environment, the mice become much more active. Importantly, no corresponding rise in dopamine accompanies exposure to the novel environment, suggesting that these behavioral changes are regulated through more than just the dopamine system. These mice also show significant cognitive impairment in an eight-arm radial maze test, a standard approach to evaluate spatial cognitive function in rodents. Specifically, the mutant animals make significantly more perseverative errors, suggesting that these mice might suffer from poor behavioral inhibition.
An obvious question is whether the drugs commonly used in the treatment of attentional difficulties have any effect on these mice. Administration of amphetamine (Adderallt, Dexedrinet), methylphenidate (Ritalint), or cocaine to the hyperactive knockout mice calms them; thus they show a response to psychostimulants that is similar to the response seen in humans with ADHD. Conversely, normal mice become hyperactive when given these psychostimulants (Fig. 1).
Normal mice show an expected increase in extracellular dopamine brain levels in response to an injection of methylphenidate, which blocks the dopamine transporter. Of interest, the knockout mice do not show any changes. These findings strongly suggest that psychostimulants do not affect the dopamine system in these mice and most likely exert their calming effects through modulation of other neurotransmitters targeted by these drugs.
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http://www.med.yale.edu/chldstdy/plomdevelop/genetics/01margen.htm

Sorry to derail the topic, but I don't think it was going too far anyway...
 
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Kolmogorov said:
Of course I did not researched it. I just posted a link. Didn't knew that posting a bloody link would make me get flamed, though.:\ But in retrospect. it was a very stupid thread that's what happen when you don't sleep for 36 hours and don't do drugs meanwhile
Click to expand...

This is "advanced" drug discussion. It's for the discussion of topics that are scientific and advanced in nature, hence the name. If you look through the other threads in this subforum, you'll see lots of very well thought out OPs and responses. If you're not willing or able to do some research yourself, don't post until you have.

You were flamed earlier, and I apologise for the way you were treated by others. It was unnecessary, and the goal could have been accomplished with more kindness.

Regulars in this forum are all very intelligent, all have a high degree of education and the majority work in some aspect of pharmacology or chemistry. Anyone can certainly learn enough to carry on an intelligent conversation here, of course. It's not exclusive by any means.

As we recently discussed in a couple other threads here, the easiest way to not get flamed is to not be lazy. Before you post, do your research.

Of course I did not researched it. I just posted a link.
Click to expand...

And that was the problem. You started a thread that really belonged in ADD, but didn't put any effort into it. It may not be 'banned' but it's a really good way to destroy your reputation around here. If you're tired, go to sleep and post later. Do some research, and then when you're rested and ready, post a thread that really belongs here. Otherwise, you're just creating homeless orphans.

And orphans don't get any love, do they? Well, at least not in Eastern Europe.

But, you're new, so just chalk it up to a lesson learned. No harm done, and I hope you're not too scared to come back with something really good.

Hammilton

Like which? Everyone here calls MDPV a selective DARI but the data I recall reading on its receptor affinity was 3:1 NET:DAT. If someone has this data and could illuminate the subject, please do! I'm also curious to the dopamine selective stimulants. So far as I can tell highly selective dopaminergic stimulants (like RTI-121) have rarely ever been tasted.
Click to expand...

I should have left it at the not neccessary part. You're right, there are very few stimulants commonly used that are dopamine specific. I'm really not a stim buff, FnB would be better able to answer this, but without doing any research, there must be at least *one* dopamine specific commonly used stimulant, no? But even still, I'll stand by my claim that NE effects aren't needed for a stimulant to be good. NARIs feel like crap, imho. Strattera, with it's primary effects as a NARI, it pretty crappy ime.

Are there any actual recreational NARIs out there?

Does anyone know if this substance has been tasted? It's a methylated version of atomoxetine. The change might make it recreational.

methylmoxetineyy2.png
 
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OK, got that. I'll bring something more interesting (and more researched!) next time :)
 
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