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!