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dopamine reuptake inhibitors

I think it has to do with the relative amounts of different monoamines that are affected. Purely dopaminergic reuptake inhibitors probably won't feel very stimulating. When you add NE and 5HT activity, you'll get a stimulant.
 
my question is meant more towards why reuptake inhibition is enough to get you high, so to say. think of how serotonine releasers will get you high, while SSRIs won't. it cannot bei just the ratio of the neurotransmitters involved, since there are also SNDRIs (TRIs), which inhibit the reuptake of serotonin, noradrenaline and dopamine and still won't get you high.
 
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A lot has to do with how fast and how completely/efficiently the drug occupies the monoamine transporter sites and blocks monoamine re-uptake. Bupropion has low transporter occupancy at normal doses about 20-30% of DAT sites, combined with relatively slow onset.

Rapid occupancy combined with efficient re-uptake inhibition leads to a surge in synaptic monoamine levels which in turn stimulates greater activity and further release of monoamines.

there more to it than the simple explanation above, but it explain most drug profiles
 
^ How fast a psychoactive drug works explains the relative abuse potential over a wide range of classes.
 
ungelesene_bettlek said:
...there are also SNDRIs (TRIs), which inhibit the reuptake of serotonin, noradrenaline and dopamine and still won't get you high.
Click to expand...

A bit tangential, but have you, by any chance, sampled a TRI, and if so which, and if so what was it like?

Bupropion is a bad example here because there is serious debate about whether or not its DRI activity is significant enough for the drug to be classified as a DRI. Also, immediate release bupropion can be intensely stimulating, especially after a few days into a 150 mg tid regimen. It also has structural attributes that give it unique properties (such as the tert-butyl group that follows and shields the amine, and the chlorine on the phenyl.

A more interesting example is Daytrana, the methylphenidate patch. It certainly lacks the rapid onset, but anecdotal reports tout it as a superior stimulant than amphetamine.

Excuse me if I'm ignoring something obvious, but there's an amphetamine patch in the works (though it remains at the preclinical trial stage). It is SPD-483, progeny of Shire. It'll be interesting to see where this one goes.
 
just got bumped up to 150mg of wellbutrin per day. hows this gonna affect the MDPV high? both being dopamine reuptake inhibitors, just one thats slow and one thats fast n stimulating :p ... stuff makes me so sadistic and emotionless...and i kinda like it :3
 
mezimomo said:
just got bumped up to 150mg of wellbutrin per day. hows this gonna affect the MDPV high? both being dopamine reuptake inhibitors, just one thats slow and one thats fast n stimulating :p ... stuff makes me so sadistic and emotionless...and i kinda like it :3
Click to expand...

I would be wary of combining bupropion with stimulants, due to risk of seizure.
 
I'd be wary too, especially if you're into high doses or smoking/shooting the MDPV.
That said, I've done a bit of mephedrone while on bupropion last year. If anything the high was less stimulating and euphoric. Generally speaking, I fell bupropion results in less satisfying highs, many people seem to agree. But that is in an extended treatment, maybe in the beginning you'll get enhanced highs. Just like I get more urges to smoke cigarettes in the beginning of a bup treatment but it all fades away after 1-2 weeks.
 
Bupropion turns extensively into hydroxy-bupropion in liver which is a NRI so it is almost a NRI in vivo while in vitro it is DRI. So it has a weak stimulant effect in vivo.
If you inhibit metabolization of bupropion with some other meds you will find it more stimulating.
 
1. not a complete list
2. "not near" statement seems silly since at least one of them is obviously clinically significant (butryptilline). Only about 3x less potent DA activity than SE, and stronger DAT than NAT.
 
Looking at this, Iprindole and Opipramol (probably but other numbers are missing) are probably better than most too. Opipramol has the sigma issues though.

Wondering- is Opipramol abused in Germany? Many Sigma agonists are abused, so I imagine that this one is too, but I have no evidence.
 
A good friend mentioned occasionally that the "person X has the typical Insidon smile", and that its an old AD/Anxiolytika/Tranquilizer. But she never implied that the person abused it, only took it for medical reasons. Altough she advised against it when I more jokingly suggested that I should take it. Never heard that its being abused here though (I'm Swiss btw).

Interesting that you mention Sigma agonists being abused, didn't know that. I only noticed that the antidepressivas working in me usually have at least some Sigma activity. 3-MeO-PCP being the latest (highly suspected) "example"...

I would guess any DRI of Opipramol would be overshadowed by its Histamin antagonsism.
 
i have a question... i was thinking about taking Fluvoxamine with Agomelatine, since Fluvoxamine inhibits CYP1A2, i would get higher levels and longer half life of Agomelatine. but i read that Fluvoxamine is a Sigma agonist, and i don't know anything about sigma.

What kind of relationship does Sigma have to dopamine, glutamate, serotonin, or other neurotransmitters? I know its antidepressant, but i was wondering how it interacted with other stuff..
 
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