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A Ritalin nite, after a adderall nite? reduced effects?

psyie

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Jul 27, 2011
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I got some adderall and ritalin, so i took 20mg of addy 1 nite, 2 stay awake. the next nite i did 40mg of ritalin.
my question is. Did the dose of adderall have any effect on the ritalin? would the adderall being in my system give the ritalin a reduced effect?
Would it be better to wait until my system is " cleaner" to take a diff drug?
Can these drugs be taken together for Rec purpose only?? How does that buzz fell 4 you?
thanks all.
Admins fell free to mod title, or move thread if its not supposed to be here.
I thought it required a bit of Advanced knowledge to answer.
Thanks all for reading and/or Posting.
 
This isn't advanced, but I will respond. Adderall phosphorates your DAT, Ritalin binds to uncompromised DAT, so yes, Adderall would reduce the effects of Ritalin the day after more than Ritalin would reduce the effects of Adderall the day after. Ritalin is a DRI which is shown to be neuroprotective, while Adderall is a DRA which is shown to be neurotoxic.

Receptor re-regulation and basic manners of tolerance may have something to do with it, with either before the other, as well too though.

Taking DRIs & DRAs together would increase the overall dopaminergic occupancy of transporters, but they're mutually exclusive in relation to individual transporters on a transporter by transporter basis: a DRA cannot phosphorate DAT that has a DRI as a ligand, and a DRI cannot bind as a ligand to DAT that has been phosphorated by DRA. Because DRAs usually have a longer elimination half-life by metabolism, the protection of the transporters given by DRIs against DRAs is negligible, and for the most part, the subjective effects of DRIs fade into the subjective effects of DRAs when administered together.
 
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wow thats a lot of big words i need to learn, But i got the basics.
If you have the power to move the thread please do, more ppl will post answers.
I do not know how to move my threads.
Thanks :)
 
In short, both drugs act to increase levels of monoamines (dopamine and norepinephrine) but they do so through different mechanisms. The end result is the experience can be very similar between the two and there is what people call "cross tolerance" - taking one drug will make you tolerant to the other and vice versa.
 
My intuition, though, is that initial use of ritalin would cause less cross-tolerance with adderall dosed subsequently than the inverse regimen, as DRIs tend not to deplete vesicular stores of monoamines as do releasers (particularly when the latter are taken at high doses). However, missing food and sleep will reduce desired response to stimulants in general.

ebola
 
My intuition, though, is that initial use of ritalin would cause less cross-tolerance with adderall dosed subsequently than the inverse regimen, as DRIs tend not to deplete vesicular stores of monoamines as do releasers (particularly when the latter are taken at high doses). However, missing food and sleep will reduce desired response to stimulants in general.

ebola

Yes this too, mostly because re-uptake does not return to normal functioning on a compromised transporters I am assuming. As well as my previous mention that transporters are internalized en mass by phosphorylization and there are therefore less of them from initial administration of a DRA for a DRI to act upon when administered later.
 
huh i dont really understand all of the DRA/DRI stuff, but i get the main point. I will study about the DRA/DRI stuff. Thanks all.
close thread or leave open?
 
DRA = dopamine releasing agent
DRI = dopamine re-uptake inhibitor

Both are indirect dopamine agonists, which mean they are not dopamine agonists i.e. they do not work on the dopamine receptors, but mediate the function of dopamine through the transporter so that dopamine itself acts as an agonist more virulently upon the receptors.

That is how they are similar.

However, DRAs compromise the transporter in such a way that dopamine freely exits and re-enters the transporter, like a two way street, from both it's normal point of exit and its normal point of entry: the re-uptake pump. This fills the synapses with free-floating dopamine.

DRIs, on the other hand, 'link up' and attach themselves to the point of re-entry for dopamine on the transporter, so that dopamine cannot come back into it, and unlike DRAs influence, the dopamine does not re-enter from the normal point of exit either, because the transporter is uncompromised. Rather it keeps the dopamine in the synapse closer to the receptors, on the opposide side of the axon/dendrite from the transporter.

Notice how one can be neurotoxic and the other neuroprotective? One 'herds' the dopamine to more confined places, the other breaks down the fence and lets them roam free. Both in a way that succeeds in getting them from a particular point A to an equally specific point B moreso than they do naturally.
 
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My intuition, though, is that initial use of ritalin would cause less cross-tolerance with adderall dosed subsequently than the inverse regimen, as DRIs tend not to deplete vesicular stores of monoamines as do releasers (particularly when the latter are taken at high doses). However, missing food and sleep will reduce desired response to stimulants in general.

ebola

Agreed.

To put it simply; Ebola is saying that in theory, had you had taken a dose of methylphenidate (a strict dopamine/norepineprine reuptake inhibitor) prior to the amphetamine (a more pharmacologically complex compound), a reduced 'effect' would be more likely.

Theory aside; based on the info you provided (unless the amphetamine was in an 'XR' formulation) any decreased effect from methylphenidate is at best nominal.
 
Agreed.

To put it simply; Ebola is saying that in theory, had you had taken a dose of methylphenidate (a strict dopamine/norepineprine reuptake inhibitor) prior to the amphetamine (a more pharmacologically complex compound), a reduced 'effect' would be more likely.

Unless I misunderstood, I believe Ebola was saying the opposite. Also, the structure of amphetamine is simpler than MPH, though I believe you mean here the mode of action or pharmacological profile rather than pharmacological structure by "pharmacologically."
 
Naglfar read my original intent correctly, but I agree with 'gesic when we're talking about cases where the DRI continues to occupy the transporter during administration of the releaser.

close thread or leave open?

This thread's fine, as we're discussing pharmacological activity in detail (even if we've discussed similar stuff before).
Mod's note: thread closure here isn't meant to express condemnation; rather, this forum is for more technical discussion rarely found in other subforums. Except for RC vendor hype-men, particularly those with fake trip reports. I condemn them. :p

ebola
 
Naglfar read my original intent correctly, but I agree with 'gesic when we're talking about cases where the DRI continues to occupy the transporter during administration of the releaser.

And it should be noted in this specific instance, with the DRI methylphenidate and DRA amphetamine, this won't be the case as MPH is shorter acting than amph.
 
Ok so I looked up what a DRI and DRA is, so i get the technical point of it now. thanks for the lesson.
I dont plan on doing these drugs back to back again, as it seemed like a waist of good drugs.
the come down wasnt bad, but i did fell kinda blah the next day.
Thanks again all who posted answers, even though some of them were backward. It still really helped.
It gave me a place to start my study.
Peace, pot, micro dot.

Quote of the nite " ppl tell me say No to Drugs. I say, If ur already talking to DruGs its probly to late" lol.
Peace out.
 
Im not an expert, not a doctor or anything. But I take adderall, and have been fascinated with drugs, trying drugs, and reading about how they work for years. anyways: ritalin(methylphenidate) is a dopamine reuptake inhibitor. It binds to the dopamine transporters (which typically suck dopamine back into the neuron that it came from)
and forms a blockade preventing dopamine from leaving the synapse to go back into the neuron that originally released the dopamine (called the pre-synaptic neuron), this ends up increasing the amount of dopamine in the synapse.amphetamine (adderall is a mixture of different salts of both isomers of amphetamine) is a dopamine reuptake inhibitor, but it is also a bit of a releasing agent as well (mostly at high doses). the dopamine releasing agent aspects are more evident at high doses, but the mechanism that it acts as a releasing agent is: it reacts with the dopamine transporter (which is a protein) , and causes it to actually work in reverse and pump more dopamine into the synapse.

anyways: both work similarly and end up increasing dopamine levels. tolerance to one of them will also create tolerance for the other one. as they are very similar
drugs. but not completely similar.
 
amphetamine (adderall is a mixture of different salts of both isomers of amphetamine) is a dopamine reuptake inhibitor, but it is also a bit of a releasing agent as well (mostly at high doses).

You have this backwards. Amphetamine is a DRA primarily, and only works as a reuptake inhibitor at high doses.
 
Please dont try to prove your point. I already studied the 2 drugs, and learned what i could understand.
Mod please close this thread.
Thanks all.
 
The way I see it - anything that acts as a direct releasing agent (i.e. reversed DAT) must therefore be a reuptake inhibitor just because the protien sure isn'ttaking up dopamine any more. I personally agree that amph is a DRI at low doses and DRA at high doses. Its effects on norepinephrine are probably a lot more significant though.
 
Thank you: this was my understanding too. I'm wondering, though: are conditions of transport reversal binary? I.e., could there be a high efficacy releasing agent which causes little reuptake inhibition?

ebola
 
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