Stimulants Reuptake inhibitor + Releaser

[DeathIndustrial88]

Is it dangerous to mix something like 60mg IR ritalin and then do m-amp about 12-24hrs later?

I imagine it would be. Could this lead to some sort of "serotonin-syndrome"-like episode but involving dopamine?

Haven't found much about mixing these two.

 

[Function]

Will it kill you? Unlikely.

Will it increase the risk of psychotic symptoms (which would be, crudely, the dopamine equivalent of seratonin syndrome, i.e. the consequence of too much dopamine bashing about in your nervous system)? Yes

Will you experience psychosis? Impossible to say, depends of history, dose, sleep, etc. etc.

 

[DeathIndustrial88]

Will it kill you? Unlikely.

Will it increase the risk of psychotic symptoms (which would be, crudely, the dopamine equivalent of seratonin syndrome, i.e. the consequence of too much dopamine bashing about in your nervous system)? Yes

Will you experience psychosis? Impossible to say, depends of history, dose, sleep, etc. etc.

Thanks Function.

I recently made the mistake of doing exactly this.

I ended up with moderate to severe "poisoning" symptoms.
Beginning with hyperreflexia, feelings like I was about convulse, loss of muscle control & coordination, spasms, tightening of the chest, etc..
Looked like strychnine poisoning symptoms honestly.

Wasn't sure if maybe it was the combo or if maybe I was given really bad stuff. The latter is also possible, but I'd rather not discuss that unless specifically asked.

 

[Skorpio]

Ritalin isn't a serotonin reuptake inhibitor, so serotonin syndrome is unlikely to occur.

However on combining ndris with releasers I've heard a number of things (usually based on affinity and quantity). If the releaser needs to be taken up a la mdma pretreatment can weaken effects. If it is something very lipophillic like m-amp it will pass through the membrane and effects will be potentiated (unsure whether additive or multiplicative; my guess would be additive.)

Amphetamines block reuptake when administered. This is not a major driver of their effects (VMAT reversal driven release is + TAAR effects that also modulate release). However, it indicates to me that adding another reuptake inhibitor would not be multiplicative.

Also anecdotally, i have combined releasers (plain amp) and reuptake inhibitors (methylphenidate or cocaine) and noticed only seemingly additive effects.

 

[Xorkoth]

I think he's talking about dopamine concerns, not serotonin.

Mixing the two is not as dangerous as mixing a serotonin reuptake inhibitor with a releaser, that is very dangerous indeed and can easily lead to serotonin syndrome. But the excess dopamine along with the inability to reuptake it properly can certainly lead to unpleasant or even dangerous outcomes.

 

[DeathIndustrial88]

Hmm.

I wonder if I truly was poisoned by somebody then.



I've actually mixed venlafaxine & meth and have been alright. And also DXM & meth. Waaay back in the day. Not saying it's safe, but I'm doubting now that a DRI + releaser did this to me, when an SSRI/SNRI + Releaser did not.

I think something else happened. Or maybe I did overdo it, I dunno.

 

[Vagabond696]

I take venlaflaxine daily and various drugs more often than I should and haven't experienced any issues.

 

[purplehaze147]

Is it dangerous to mix something like 60mg IR ritalin and then do m-amp about 12-24hrs later?

I imagine it would be. Could this lead to some sort of "serotonin-syndrome"-like episode but involving dopamine?

Haven't found much about mixing these two.

Good question. The pharmacology behind amphetamines (TAAR1 agonists and VMAT2 inhibitors) and NDRI's/SNDRI's suggests they are not additive anywhere near as much as you'd think.

Monoamine reuptake inhibitors actually prevent a significant amount of the particular amphetamine from reaching their main target receptor, the TAAR1, which is located within the presynaptic neuron. Normally an amphetamine would go through the reuptake transporter to reach it, but the reuptake inhibitor will blocking the path inside. Amphetamines can passively diffuse through the membrane of the presynaptic neuron, but only to a small degree. And even when they do, activation of the TAAR1 reverses the reuptake transporters' directional flow to release dopamine, noradrenaline, and/or serotonin into the synapse instead of normally sucking them back in from the synapse allowing them to reach the other side of the synapse where their receptors are located on the post synaptic neurons. But again, the reuptake inhibitor is blocking their release by this path.

Not all reuptake transporters will be saturated, so there will be some added stimulation, but as you can see they're not good to mix and they render much of the amphetamine unable to reach its receptor.

This can be shown by SSRI's pretty much totally blocking MDMA's entactogen property. MDxx have the greatest affinity for TAAR1's in the serotonin neurons, while amphetamine has the greatest affinity to dopamine and noradrenaline neurons, and methamphetamine is pretty balanced between the three. Dopamine is mainly causing the euphoria for amphetamine and methamphetamine, and NDRI's normally have already noticable stimulate effects pretty similar to dopamine and noradrenaline releasers unlike SRI's compared to serotonin preferring releasers like MDxx's, fenfluramine, PMMA (the latter two are not really pleasent like most most selective serotonin releasers - MDxx's are triple monoamine releasers with only a preference for serotonin release and also 5HT2A agonists).

 

[izo]

no problem witho 5ht, but with 60mg Ritalin I’d sleep a night before doing meth. So it’s more like 24hrs later taking the meth.

 

[DeathIndustrial88]

Good question. The pharmacology behind amphetamines (TAAR1 agonists and VMAT2 inhibitors) and NDRI's/SNDRI's suggests they are not additive anywhere near as much as you'd think.

Monoamine reuptake inhibitors actually prevent a significant amount of the particular amphetamine from reaching their main target receptor, the TAAR1, which is located within the presynaptic neuron. Normally an amphetamine would go through the reuptake transporter to reach it, but the reuptake inhibitor will blocking the path inside. Amphetamines can passively diffuse through the membrane of the presynaptic neuron, but only to a small degree. And even when they do, activation of the TAAR1 reverses the reuptake transporters' directional flow to release dopamine, noradrenaline, and/or serotonin into the synapse instead of normally sucking them back in from the synapse allowing them to reach the other side of the synapse where their receptors are located on the post synaptic neurons. But again, the reuptake inhibitor is blocking their release by this path.

Not all reuptake transporters will be saturated, so there will be some added stimulation, but as you can see they're not good to mix and they render much of the amphetamine unable to reach its receptor.

This can be shown by SSRI's pretty much totally blocking MDMA's entactogen property. MDxx have the greatest affinity for TAAR1's in the serotonin neurons, while amphetamine has the greatest affinity to dopamine and noradrenaline neurons, and methamphetamine is pretty balanced between the three. Dopamine is mainly causing the euphoria for amphetamine and methamphetamine, and NDRI's normally have already noticable stimulate effects pretty similar to dopamine and noradrenaline releasers unlike SRI's compared to serotonin preferring releasers like MDxx's, fenfluramine, PMMA (the latter two are not really pleasent like most most selective serotonin releasers - MDxx's are triple monoamine releasers with only a preference for serotonin release and also 5HT2A agonists).

Wow, really, thank you for explaining this further!!!

Wait, amphetamines are VMAT2 inhibitors? Wouldn't this shut off a persons ability to have religious/mystic experiences while on them?
Or is the whole VMAT2 gene thing just fiction?



I originally asked this because I did 60mg IR methylphenidate & then did m-amp about 12-24hrs later, awhile back.
I remember feeling the m-amp and getting the usual "omg I'm ready to get it on" feeling I get from it.
but then the person gave me some to have from a different bag, which I think was cut with (or straight up) strychnine or something, because upon doing it, I noticed stimulation, but no horniness.
Which tells me it wasn't real m-amp. M-amp should always have me feeling horny.
Then I started having hyperreflexia, felt like I was burning, eventually felt like I was gonna have convulsions.
Thankfully I had enough benzos to save my ass, but needless to say, that "free shit" went in the trash.
Think the person did it on purpose because I wouldn't sleep with them.

Thought maybe it was the fact that I mixed the 60mg with the other stuff & maybe over did it, but I'm not so sure that's all it was.

Thanks for all this information, purplehaze!

 

[izo]

And regarding mixing these two I’d start with the mph and then add vaped meth, I think this is the best you can make out of it.

 

[purplehaze147]

Wow, really, thank you for explaining this further!!!

Wait, amphetamines are VMAT2 inhibitors? Wouldn't this shut off a persons ability to have religious/mystic experiences while on them?
Or is the whole VMAT2 gene thing just fiction?



I originally asked this because I did 60mg IR methylphenidate & then did m-amp about 12-24hrs later, awhile back.
I remember feeling the m-amp and getting the usual "omg I'm ready to get it on" feeling I get from it.
but then the person gave me some to have from a different bag, which I think was cut with (or straight up) strychnine or something, because upon doing it, I noticed stimulation, but no horniness.
Which tells me it wasn't real m-amp. M-amp should always have me feeling horny.
Then I started having hyperreflexia, felt like I was burning, eventually felt like I was gonna have convulsions.
Thankfully I had enough benzos to save my ass, but needless to say, that "free shit" went in the trash.
Think the person did it on purpose because I wouldn't sleep with them.

Thought maybe it was the fact that I mixed the 60mg with the other stuff & maybe over did it, but I'm not so sure that's all it was.

Thanks for all this information, purplehaze!

VMAT2 stands for vesicular monoamine transporter type-2. It moves monoamines into synaptic vesicles, little storage bubbles of monoamines within the presynaptic neuron that get released by exocytosis. Amphetamines inhibit it, allowing for monoamines to be released through the reversed transporter (that reuptake inhibitors block). So the pharmacology really clashes between releasers that use TAAR1 and monoamine reuptake inhibitors. I don't see why it would shut off a mystic experience. DMT and certain other powerful psychedelics have fairly high affinity for the TAAR1.

 

[DeathIndustrial88]

VMAT2 stands for vesicular monoamine transporter type-2. It moves monoamines into synaptic vesicles, little storage bubbles of monoamines within the presynaptic neuron that get released by exocytosis. Amphetamines inhibit it, allowing for monoamines to be released through the reversed transporter (that reuptake inhibitors block). So the pharmacology really clashes between releasers that use TAAR1 and monoamine reuptake inhibitors. I don't see why it would shut off a mystic experience. DMT and certain other powerful psychedelics have fairly high affinity for the TAAR1.

There was a 'conspiracy' video circulating awhile back about scientists using a vaccine to inhibit VMAT 2 to reduce religious extremism. Wasn't sure of it's validity since I don't know much in that field.

Experimenting with Spirituality: Analyzing The God Gene in a Nonmajors Laboratory Course

References linking genes to complex human traits, such as personality type or disease susceptibility, abound in the news media and popular culture. In his book The God Gene: How Faith is Hardwired into Our Genes, Dean Hamer argues that a variation in ...

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