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I've never really seen it talked about on here, so I'll make a start. I'll put some cool pictures in-between, this is both for you and I.
PRL-8-53 (I'm going to call it PRL for short) is a compound based upon the phenethylamine structure. Phenethylamine (PEA), for any other nootropic boyos, is a CNS stimulant, which acts as a neuromodulator (regulates nerve activity) by binding to TAAR1 and modulating monoamines (dopamine, serotonin, etc). This thread won't be about PEA, because PRL mogs to oblivion.
I'll just state the two main neurological mechanisms, and talk about each separately (structuring king): Dopaminergic neurotransmission and cholinergic neurotransmission. Just a disclaimer, quite a lot of this is coming from limited studies, and a majority of it will be coming from my own speculation. Sorry lads, blame the Jews for gatekeeping.
Dopaminergic neurotransmission - Contrary to dogmatic belief on the forum, a majority of your dopamine isn't produced in your brain. This isn't necessarily a bad thing, as dopamine isn't just happy fuel for your brain. It allows for survival-based feedback loops in your kidneys (notably sodium excretion), and the gastrointestinal tract (bicarbonate secretion, gut motility, and sodium transport). In an ideal world, where each human has an ideal microbiome, this is completely fine (50% to the brain, 50% to the rest of the body). However, modern diets require us to subvert more dopamine to extra-cerebral tissue. I'm not sure on an exact estimate, but lets say for the sake of the argument 30/70. This is why we're all so depressed and unmotivated nowadays, we literally do not have the same amount of dopamine flowing through our brain. This is why I believe many (in this generation) turn to dopaminergic drugs. PRL acts as a dopaminergic receptor agonist. This basically means that it mimics dopamine (in the brain), thus stimulating their natural ligand, and causing a neural connection.
Cholinergic neurotransmission - Choline is the biosynthetic precursor of acetylcholine (ACh). ACh functions as a neurotransmitter used at a neuromuscular junction (point between motor neurones and muscle fibers). The conversion process (acetylation) occurs in the terminal point of the motor neurones (presynaptic terminals). Basically, ACh is the reason that your muscles move in command with your brain (very important). ACh, alone has a lot of indirect mechanisms on it own that promote memory/learning efficiency (promoting REM sleep, alertness when we first awake, sustaining attention, etc), but I'll speak about its direct mechanism: stimulating the nicotinic (enhance encoding of new memories) or muscarinic (enhances working memory) receptors. I'm not going to go into depth on how each receptor works, but nicotinic receptors work by hastening depolarisation (neurons fire around faster), and muscarinic receptors work by improving synaptic plasticity (how new neurones strengthen connections), and enhances long-term potentiation (forming longer-stored memories). Naturally, humans produce a small amount of choline in the liver via the phosphatidylethanolamine, so most of our choline comes from diet. Yet again, our diet is fucked. We don't eat enough eggs, liver, red meat, etc. But PRL, similarly to dopaminergic receptors, acts as a agonist in the cholinergic neurons. Mazel tov!
There we go. Obviously, PRL Increases Brain-Derived Neurotrophic Factor (BDNF) and Nerve Growth Factor (NGF), but this is very common for nootropics of this nature, so I decided to not really comment on them. If you are to experiment with PRL-8-53, you should take roughly 5mg a day before cognitively demanding tasks (as it has a half-life of around 4 hours). Okay, I'm done. I'm not really bothered with proper formatting.
@apatheia @Blackpillirony @Schizotypalcel @TonyDr @Enrique ꗞ @BigDihDiddy
PRL-8-53 (I'm going to call it PRL for short) is a compound based upon the phenethylamine structure. Phenethylamine (PEA), for any other nootropic boyos, is a CNS stimulant, which acts as a neuromodulator (regulates nerve activity) by binding to TAAR1 and modulating monoamines (dopamine, serotonin, etc). This thread won't be about PEA, because PRL mogs to oblivion.
I'll just state the two main neurological mechanisms, and talk about each separately (structuring king): Dopaminergic neurotransmission and cholinergic neurotransmission. Just a disclaimer, quite a lot of this is coming from limited studies, and a majority of it will be coming from my own speculation. Sorry lads, blame the Jews for gatekeeping.
Dopaminergic neurotransmission - Contrary to dogmatic belief on the forum, a majority of your dopamine isn't produced in your brain. This isn't necessarily a bad thing, as dopamine isn't just happy fuel for your brain. It allows for survival-based feedback loops in your kidneys (notably sodium excretion), and the gastrointestinal tract (bicarbonate secretion, gut motility, and sodium transport). In an ideal world, where each human has an ideal microbiome, this is completely fine (50% to the brain, 50% to the rest of the body). However, modern diets require us to subvert more dopamine to extra-cerebral tissue. I'm not sure on an exact estimate, but lets say for the sake of the argument 30/70. This is why we're all so depressed and unmotivated nowadays, we literally do not have the same amount of dopamine flowing through our brain. This is why I believe many (in this generation) turn to dopaminergic drugs. PRL acts as a dopaminergic receptor agonist. This basically means that it mimics dopamine (in the brain), thus stimulating their natural ligand, and causing a neural connection.
Cholinergic neurotransmission - Choline is the biosynthetic precursor of acetylcholine (ACh). ACh functions as a neurotransmitter used at a neuromuscular junction (point between motor neurones and muscle fibers). The conversion process (acetylation) occurs in the terminal point of the motor neurones (presynaptic terminals). Basically, ACh is the reason that your muscles move in command with your brain (very important). ACh, alone has a lot of indirect mechanisms on it own that promote memory/learning efficiency (promoting REM sleep, alertness when we first awake, sustaining attention, etc), but I'll speak about its direct mechanism: stimulating the nicotinic (enhance encoding of new memories) or muscarinic (enhances working memory) receptors. I'm not going to go into depth on how each receptor works, but nicotinic receptors work by hastening depolarisation (neurons fire around faster), and muscarinic receptors work by improving synaptic plasticity (how new neurones strengthen connections), and enhances long-term potentiation (forming longer-stored memories). Naturally, humans produce a small amount of choline in the liver via the phosphatidylethanolamine, so most of our choline comes from diet. Yet again, our diet is fucked. We don't eat enough eggs, liver, red meat, etc. But PRL, similarly to dopaminergic receptors, acts as a agonist in the cholinergic neurons. Mazel tov!
There we go. Obviously, PRL Increases Brain-Derived Neurotrophic Factor (BDNF) and Nerve Growth Factor (NGF), but this is very common for nootropics of this nature, so I decided to not really comment on them. If you are to experiment with PRL-8-53, you should take roughly 5mg a day before cognitively demanding tasks (as it has a half-life of around 4 hours). Okay, I'm done. I'm not really bothered with proper formatting.
@apatheia @Blackpillirony @Schizotypalcel @TonyDr @Enrique ꗞ @BigDihDiddy
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