1,3-Dimethylamylamine, “Geranamine”, mimics norepinephrine enough to bind to the norepinephrine reuptake transporter, but not enough to be taken up. Therefore, 1,3-Dimethylamylamine blocks the transporter, causing a buildup of norepinephrine in the synapse because it is not inactivated by reuptake. 1,3-Dimethylamylamine, like amphetamines, releases norepinephrine from nerve endings by converting the norepinephrine transporters into open channels (1). In fact, 1,3-Dimethylamylamine is more adrenergic than methamphetamine or amphetamine, but far less dopaminergic than the two (2). The more adrenergic, the more it mimics epinephrine. A study done in 1946 also shows this characteristic of 1,3-Dimethylamylamine. The study titled, Comparison Of Pressor Action Of Aliphatic Amines tested 46 different aliphatic amines on dogs, and out of the 46, 1,3-Dimethylamylamine was the most potent (3). Sounds a lot like AMP now doesn’t it? The bottle even says “adrenaline mimetic” right there on the front. Out of all the 46 different aliphatic amines, 1,3-Dimethylamylamine was most like epinephrine in intensity of action (3). It’s easy to see that PA was looking for a “revolutionary energy/fat loss formula” as it says on the bottle, and if you try to think like him for a moment, you too would want to come up with a compound that mimics adrenaline the best as an ephedra replacement. That compound is 1,3-Dimethylamylamine. Merck & Co., Inc. classifies 1,3-Dimethylamylamine as an a-adrenergic agonist (10). What is an a-adrenergic agonist? It is an adrenaline like drug that acts on the alpha-adrenergic receptor which causes vasoconstriction, uterine contractions, and mydriasis. Patrick Arnold said this about Geranamine, “I don't know details on what types of neurons this stuff effects in the brain. i really just know (and it has been documented) that it exhibits the classic peripheral effects of catecholamines in the body- tachycardia, pressor effects [see 1946 study above], mydriasis, etc. etc.” (5) On the same post, user “Zazou” thanks PA because he no longer has to take Provigil because AMP seems to work the same to him when he stays up late working. Provigil is also an alpha-adrenergic drug with more central effects compared to 1,3-Dimethylamylamine’s more peripheral effects (6). Sympathomimetic adrenergic agents produce their effects by 5 different mechanisms:
1. Direct stimulation of the alpha- and beta-adrenergic receptors
2. Indirect release of norepinephrine from the presynaptic cytoplasm through a process
that bypasses exocytosis.
3. Direct stimulation of adrenergic receptors and an indirect release of presynaptic norepinephrine.
4. Prevention of presynaptic uptake of norepinephrine. By preventing uptake, norepinephrine concentration
rises in the synapse, leading to excessive stimulation of adrenergic receptors.
5. Prevention of norepinephrine metabolism. As norepinephrine is mainly metabolized by the enzyme
monoamine oxidase, the monoamine oxidase inhibitors (MAOIs) are the class of drugs that produce their
sympathomimetic effects through this final mechanism (7).
So then where is all the euphoria? That’s where we meet dopamine. If amphetamines and methamphetamine are way more potent as dopaminergics than 1,3-Dimethylamylamine, where does all the euphoria come from (2)? 1,3-Dimethylamylamine is placed in the opposite spectrum, being more adrenergic remember(2)? And why is (was) AMP’s euphoria superior than euphoria from addies or meth, with the latter being way more dopaminergic? At first it doesn’t seem to make sense at all. There is definitely a dopaminergic aspect to this compound which any AMP responder can vouch for.
That brings us to the relationship of dopamine and norepinephrine. They already have a link, they both are synthesized from L-Tyrosine. Recent studies show that the co-release of dopamine and norepinephrine are controlled by alpha-receptors located on norepinephrine nerve terminals.
Extracellular NA concentrations were found to be similar in the different cortices, as expected from the homogeneous NA innervation, however, unexpectedly, also DA concentrations in the PFC were not significantly different from those in the other cortices. The alpha(2)-adrenoceptor agonist clonidine, intraperitoneally (i.p.) injected or locally perfused into the PFC, reduced not only extracellular NA levels, as expected from its ability to inhibit NA neuron activity, but also markedly reduced extracellular DA levels. Conversely, the alpha(2)-adrenoceptor antagonist idazoxan, i.p. injected or locally perfused into the PFC, not only increased extracellular NA levels, in line with its ability to activate NA neuron activity, but also increased those of DA (8). {NA=noradrenaline, DA=dopamine}
and from the same article:
Our results suggest that extracellular DA in the PFC, as well as in the other cortices, may depend on NA rather than DA innervation and activity. They suggest that dialysate DA reflects the amine released from NA neurons as well, where DA acts not only as NA precursor but also as co-transmitter. The co-release of NA and DA seems to be controlled by alpha(2)-receptors located on NA nerve terminals (8).
from another article published a few years before the previous article:
There is growing evidence of an interaction between dopamine and norepinephrine. To test the hypothesis that norepinephrine terminals are involved in the uptake and removal of dopamine from the extracellular space, the norepinephrine uptake blocker desmethylimipramine (DMI) was infused locally while the extracellular concentrations of dopamine were simultaneously monitored. DMI increased the extracellular concentrations of dopamine in the medial prefrontal cortex and nucleus accumbens shell but had no effect in the striatum. The combined systemic administration of haloperidol and the local infusion of DMI produced an augmented increase in extracellular dopamine in the cortex compared with the increase produced by either drug alone. This synergistic increase in dopamine overflow is likely due to the combination of impulse-mediated dopamine release produced by haloperidol and blockade of the norepinephrine transporter. No such synergistic effects were observed in the nucleus accumbens and striatum. Local perfusion of the alpha2-antagonist idazoxan also increased the extracellular concentrations of dopamine in the cortex. Although the stimulation of extracellular dopamine by idazoxan and DMI could be due to the increased extracellular concentrations of norepinephrine produced by these drugs, an increase in dopamine also was observed in lesioned rats that were depleted of norepinephrine and challenged with haloperidol. This contrasted with the lack of an effect of haloperidol on cortical dopamine in unlesioned controls. These results suggest that norepinephrine terminals regulate extracellular dopamine concentrations in the medial prefrontal cortex and to a lesser extent in the nucleus accumbens shell through the uptake of dopamine by the norepinephrine transporter (9).
Now if 1,3-Dimethylamylamine is acting like it is described on paper, then its highly adrenergic nature would be creating a lot of norepinephrine. According to the articles above, this extracellular increase in norepinephrine wouldn’t come without a similarly equal increase in extracellular dopamine. AMP works fairly fast, the norepinephrine aspect of it, however the dopamine aspect may take a bit longer because it is acting independently on it (AMP creates norepinephrine release while Geranamine blocks the norepinephrine transporter) and the body sees this higher extracellular level of NE and increases dopamine to match it). Now if dopamine was used to being taken up by the norepinephrine transporter, but now that transporter is blocked, it creates an effect like cocaine. Think about it. A fast release of NE which releases more DA and all this time the DA was being partially picked up by the NE transporter which is now blocked. First of all, there will be more extracellular DA, and second, it will remain in the synapses longer until the NE transporters are “unblocked” or the DA transporter picks up the rest of the extracellular DA.
Brooklynjuice’s magic addition to AMP was a synthetic harmaline derivative that hasn’t been completely singled out yet. It acts as an MAO-Inhibitor. This is one way to keep the dopamine in the synapses longer.
Could it be that the reason why 1,3-Dimethylamylamine was more euphoric than meth was because that in the end, the 1,3-Dimethylamylamine created more DA indirectly through massive amounts of NE more quickly and prevented its uptake [through NE transporters] just as fast? As I discussed above, 1,3-Dimethylamylamine mimics adrenaline well, and it appears that it creates more NE than meth or adderall would (2). So in a way you are getting the best of both worlds with 1,3-Dimethylamylamine. On paper it is not very dopaminergic, but after it creates all the NE, the body matches its NE levels with DA. And that DA level that comes after the NE increase appears to be greater than that which meth or amphetamines DA level could bring or that it happens in a faster time frame, causing the euphoria.
So as you can see, 1,3-Dimethylamylamine seems like a very likely candidate for being Geranamine.
1. http://en.wikipedia.org/wiki/Amphetamines
2. photo attachment
3. http://toxnet.nlm.nih.gov/ search by CAS# 105-41-9 to bring up study.
4. http://www.mindandmuscle.net/forum/index.p...5&hl=peripheral
5. http://www.musclegurus.com/forum/viewtopic.php?t=46
6. http://www.pharmacorama.com/en/Sections/Ca...lamines_5_1.php
7. http://www.emedicine.com/emerg/byname/toxi...athomimetic.htm
8. http://www.biopsychiatry.com/noradren-dopamine.htm
9. http://www.biopsychiatry.com/nordop.htm
10.http://www.merckbooks.com/mindex/pdf/Therapeutic category index.pdf
