For NightDancer

How the Uridine Stack Works

The uridine stack works through two main mechanisms to provide therapeutic and nootropic effects.

1.The chemical uridine promotes the creation of new dopamine receptors in the brain, an effect which is more pronounced in brains with fewer dopamine receptors. This is done by activating the D1 and D2 receptor signaling cascade, which stabilizes spikes of dopamine activity that would normally “burn out” receptors and reduce their effective number. Modulation also increases the rate of new receptor formation in areas where they are less dense, effectively increasing the number and density of dopamine receptors. Choline – particularly CDP-choline – also has the potential to increase dopamine receptor density.

2.The stack as a whole supports growth of neural tissue and the protective phospholipid material around it. Having a well-connected and healthy set of dendritic pathways in the brain can improve both mood and cognition, because functionality is optimized or restored.

Uridine research

Some of the details surrounding the mechanisms of the stack come from clinical trials and animal research, which show positive feedback for the combination in a variety of applications.

Dopamine Balance

In a study done at Rutgers University, researchers measured rats’ performance on behavioral tests after being given cocaine or amphetamines. In an experimental group that was also given uridine, the rats reacted much more sensitively to the illicit dopamine-stimulating drugs, demonstrating that the population of dopamine receptors was denser. Another observation with the uridine group was that amphetamines did not raise striatal dopamine levels as much as with the placebo group, because of the balancing effect provided by modulation.

A study done in France provided further evidence for uridine’s benefit for dopamine levels. Scientists found that rats given uridine monophosphate had a higher rate of potassium-mediated dopamine release, as well as an increased rate of neurite growth.

1 Reply

  • Notice the last paragraph, last line, where it talks about the rats' "potassium-mediated dopamine release." I believe what that means is that the scientists used potassium (as they usually do in dopamine experiments) to cause a release of dopamine in the rats. But the rats that were also fed Uridine had a greater release of dopamine than controls because the Uridine gave them bigger and better dopamine receptors from which to hurl out the dopamine. My point is, potassium in the right amount and right form (and right time), just might cause a release of dopamine in humans as well. Most good things come with a price. I see no reason why potassium can't cause augmentation eventually and down-regulate our receptors. So maybe, just maybe, Uridine might have a protective effect. That, or intermittent fasting and/or exercise.

    Hopefully (fingers and toes crossed) occasional fasting, exercise or Uridine (for the lazy man) may make our receptors so much like other people's that we don't need Rogatine or Potassium or Opiates. Unlike Parkinson's patients, we with RLS have so much dopamine kicking around in our brains we don't know what to do with it all. I mean literally, our brains don't know what to do with it all, because of our small receptors that can't quite hurl enough of that dopamine down our spines and to our legs. But once our receptors are more normal size and number, then zzzzzzzzzz!!!

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