# potentiation of stimulants with selegiline (l-deprenyl)



## martyboi (Sep 18, 2009)

Has anyone tried to potentiate their stimulants with selegiline? I've read that selegiline can potentiate stimulants exponentially, make them last longer and ease the crash and even prevent neurotoxicity.... i realize theres a risk of overstimulation and hyperthermia but i'm pretty experienced with drugs and i'm planning to carefully administer small amounts of each drug until i find a good ratio. If anyone has experience with this, please share your experience, what dose you took of each and how often...

I'm considering experimenting with low doses of selegiline like 1-2mg every other day...and 2.5mg of ritalin twice per day.


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## TimmyT999 (Mar 16, 2010)

i've heard selegiline potentiates ritalin quite a bit.


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## crayzyMed (Nov 2, 2006)

When your carefull it should work.


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## IllusionalFate (Sep 10, 2008)

Doesn't work. I tried both Adderall and Dexedrine (amphetamine) AND methylphenidate augmented with 5mg and 10mg selegiline... the adrenergic effects are potentiated, especially (or maybe even only) with amphetamine. But no potentiation of dopaminergic effects was observed under both NDRI and NDRA.


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## euphoria (Jan 21, 2009)

IllusionalFate said:


> Doesn't work. I tried both Adderall and Dexedrine (amphetamine) AND methylphenidate augmented with 5mg and 10mg selegiline... the adrenergic effects are potentiated, especially (or maybe even only) with amphetamine. But no potentiation of dopaminergic effects was observed under both NDRI and NDRA.


That would make sense - Ritalin would block the amphetamine metabolites NRA action with amphetamine by being an NRI, but selegiline would boost the adrenergic effects of amph by contributing its (un-blocked) NRA metabolites.


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## TimmyT999 (Mar 16, 2010)

Selegiline's metabolites are left isomer amphetamines which have a tough time crossing the blood brain barrier to begin with. Selegiline's primary mechanism of action is through stimulation of B-Phenylethylamine or prevention of its breakdown rather. Although I'd agree selegiline has decent adrenergic effects, which isn't always a bad thing. If you look at the stronger DRIs like ritalin and MDPV this is where you see (for some)panic attacks, anxiety, etc. Dopamine directly activates the sympathetic nervous system through innervation in the striatum so more is not always better. Then again, some people respond better to DRIs. Only way to find out is by trying it. Selegiline is strongly selective for the MAO-B isoenzyme so I wouldn't worry about MAOI interactions if you keep the dose under 10 mg.


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## euphoria (Jan 21, 2009)

Yeah, selegiline strongly boosts PEA precursors (like DLPA) and PEA itself.


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## IllusionalFate (Sep 10, 2008)

euphoria said:


> That would make sense - Ritalin would block the amphetamine metabolites NRA action with amphetamine by being an NRI, but selegiline would boost the adrenergic effects of amph by contributing its (un-blocked) NRA metabolites.


How do you explain the adrenergic potentiation of amph with no DA potentiation though? Theoretically, DA should be boosted more since MAO-B is incapacitated.



TimmyT999 said:


> Selegiline's metabolites are left isomer amphetamines which have a tough time crossing the blood brain barrier to begin with. Selegiline's primary mechanism of action is through stimulation of B-Phenylethylamine or prevention of its breakdown rather. Although I'd agree selegiline has decent adrenergic effects, which isn't always a bad thing. If you look at the stronger DRIs like ritalin and MDPV this is where you see (for some)panic attacks, anxiety, etc. Dopamine directly activates the sympathetic nervous system through innervation in the striatum so more is not always better. Then again, some people respond better to DRIs. Only way to find out is by trying it. Selegiline is strongly selective for the MAO-B isoenzyme so I wouldn't worry about MAOI interactions if you keep the dose under 10 mg.


The levoratory amphetamine metabolites are too small a dose to induce much of any effect at all, at least in comparison to common doses of Ritalin and MDPV. The reason these are anxiogenic is because of their increase in norepinephrine, not dopamine.


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## euphoria (Jan 21, 2009)

IllusionalFate said:


> How do you explain the adrenergic potentiation of amph with no DA potentiation though? Theoretically, DA should be boosted more since MAO-B is incapacitated.


Because selegiline sucks.


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## IllusionalFate (Sep 10, 2008)

euphoria said:


> Because selegiline sucks.


It does indeed.


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## euphoria (Jan 21, 2009)

It can be useful in some circumstances though. One is using a very low dose for health benefits. In terms of mood effects, I still think the selegiline + low dose DLPA, or selegiline + low dose Ritalin ideas may have some potential. Results are conflicting. I've heard reports of it not helping at all, reports of making the effects worse, and reports of it inducing euphoria so strong the user became manic and got into trouble. I dunno. But selegiline alone, or in combination with NDRAs, sucks it would seem (the latter based on your report).


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## crayzyMed (Nov 2, 2006)

euphoria said:


> It can be useful in some circumstances though. One is using a very low dose for health benefits. In terms of mood effects, I still think the selegiline + low dose DLPA, or selegiline + low dose Ritalin ideas may have some potential. Results are conflicting. I've heard reports of it not helping at all, reports of making the effects worse, and reports of it inducing euphoria so strong the user became manic and got into trouble. I dunno. But selegiline alone, yeah that sucks.


I think the health benefits of deprenyl are rather questionable and that at this point there's no way to tell wheter we are on the right side of the dose response curve.
When dosed too high it actually REDUCES the antioxidant enzymes and shortens lifespan.

The increased mortality of parkinson patients also questions the safety of this so called life extension compound.


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## TimmyT999 (Mar 16, 2010)

IllusionalFate said:


> The levoratory amphetamine metabolites are too small a dose to induce much of any effect at all, at least in comparison to common doses of Ritalin and MDPV. The reason these are anxiogenic is because of their increase in norepinephrine, not dopamine.


Are you agreeing with me? I'm not really sure what you're saying here.


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## IllusionalFate (Sep 10, 2008)

TimmyT999 said:


> Are you agreeing with me? I'm not really sure what you're saying here.


I agree with most or all of your points. It just sounded like you were implying MDPV and methylphenidate induced panic/anxiety because they're strong DRIs, when it's actually norepinephrine that's responsible for the anxiogenic effects.


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## meyaj (Sep 5, 2009)

IllusionalFate said:


> How do you explain the adrenergic potentiation of amph with no DA potentiation though? Theoretically, DA should be boosted more since MAO-B is incapacitated.


To be fair, the only evidence I've seen you cite as such is your own personal "feeling" for the neurotransmitters, which is far from scientific.

I will say though that Parnate works great in combination with Dexedrine, increasing potency and extending duration.


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## jim_morrison (Aug 17, 2008)

rocknroll714 said:


> I believe this is because MAO-B is localized in certain dopaminergic areas of the brain like the nigrostriatal pathway which is implicated in motor control (hence its use in Parkinson's disease) but that it's either scarce or non-existent in the mesolimbic pathway (and perhaps mesocortical as well) where things like pleasure, drive, and anxiolysis are mediated.


What about when dopamine is boosted in the frontal cortex, what actions does it primarily have there? and which pathway is it linked too from that area?


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## jim_morrison (Aug 17, 2008)

rocknroll714 said:


> I'm not really sure actually.. the prefrontal cortex is a very complicated part of the brain. It's involved in all kinds of stuff.. cognition, memory, mood, executive control (related to impulsivity in ADHD), attention, and motivation, among others. Even psychedelics are believed to exert their effects by acting on this area. To my knowledge it's sort of the bridge between the cortexes and the limbic system, so obviously a lot of stuff goes on there. I do know that both the mesolimbic and mesocortical pathways project to it though, but what dopamine does exactly in the area I can't tell you.
> 
> * goes off to study *


It mystifies me too, I look forward to your findings.


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## jim_morrison (Aug 17, 2008)

rocknroll714 said:


> * ...too lazy to study /heh *


Lol, I'll give you an extension then , just kidding it's all good, I'll look into it when i get around to it.


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