18% Increase in Dopamine Receptors Anyone?

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18% Increase in Dopamine Receptors Anyone?

Postby figflower » Mon Oct 05, 2015 7:04 am

Here's a summary of an experiment on dopamine receptors:

Changes in brain striatum dopamine and acetylcholine receptors induced by chronic CDP-choline treatment of aging mice.R. Giménez, J. Raïch, and J. AguilarDepartment of Biochemistry, Faculty of Pharmacy, University of Barcelona, Spain.
Abstract1. Spiroperidol binding (dopamine D2 receptors) and quinuclidinyl benzilate binding (muscarinic receptors) in striata of 19-month old mice was analyzed for animals that had received chronic administration of cytidine 5'-diphosphocholine (CDP-choline) incorporated into the chow consumed (100 or 500 mg kg-1 added per day) for the 7 months before they were killed.

2. Treated animals displayed an increase in the dopamine receptor densities of 11% for those receiving 100 mg kg-1 and 18% for those receiving 500 mg kg-1 as compared to the control aged animals that had received no CDP-choline. Control animals showed, from 2 months to 19 months of life, a 28% decrease in the receptor density. No change in the affinity of the receptors for spiroperidol was found in the treated or untreated animals.

3. Muscarinic acetylcholine receptor densities were also partially recovered by the same treatment in aged animals that showed a 14% decrease of these receptors in this case. The muscarinic receptor density increased 6% for the animals that received 100 mg kg-1 and 17% for the animals that received 500 mg kg-1 without any change in the affinity of the receptor for quinuclidinyl benzilate.

4. Aged animals displayed a slight increase in brain membrane fluidity as indicated by a decrease in the polarization value of the non-polar fluorophore 1,6-diphenyl-1,3,5-hexatriene. Interestingly, in the treated animals a greater increase in membrane fluidity was determined and found to be very similar for the two doses.

5 It is concluded that chronic administration of CDP-choline to aged animals promoted a partial
recovery of the striatum dopamine and acetylcholine receptor function normally reduced with aging,
which might be explicable in terms of mechanisms involving fluidity of the brain neuronal membrane.

Keywords: Muscarinic receptor; dopamine D2 receptor; aging; striatum; choline donor; CDP-choline (cytidine
5'-diphosphocholine); membrane fluidity


The above article is all well and good. I took CDP Choline and another substance called Uridine 5 Monophospate for three nights (several nights apart) and got terrible RLS each night, just like when I took melatonin. I would take iron to get rid of the RLS, but then four hours later I would awaken and have to repeat the iron. Which is basically unheard of for me. I thought it was the Uridine. And it might be, or it might be the Choline or the combination of the two. Both these substances increase acetylcholine in the brain supposedly which kind of, sort of, might antagonize the dopamine system if too much of the acetylcholine is kicking around up there. There are two kinds of drugs they give to Parkinson's patients, one that increases dopamine in the brain or one that inhibits acetylcholine. So maybe my ultra sensitive RLS brain couldn't handle that increase in acetylcholine and what ever tiny drop of an affect it had on my dopamine transport. By the way, I take acetylcholine by day (I try for twice a day). It is the only substance I have found (in 40 years of searching) that increases peristalsis in the lower gut without causing diarreah or cramping. When we take DAs we tend to get constipated, right, because the release of dopamine in the gut slooooooooows everything down. And if we take anti-emetics which increases peristalsis (maybe by blocking dopamine in the gut) it aggravates our RLS. Yet somehow the acetylcholine I take by day does not seem to trigger my RLS whereas the CDP choline and/or the Uridine which increases acetylcholine does??? Everyone following me :|

My point is, these substances are not a quick fix and if taken at night might even be a nightmare, but in the long run are supposed to increase the number and density of our receptors. There are several similar experiments out there where they "pre-treat" mice with Uridine for several weeks or months and then they induce the release of dopamine in these mice (and control mice) with potassium. Like I said, potassium is great at causing a quick large dopamine response. Anyways, the mice that were "pre-treated" with Uridine had a much greater potassium evoked release of dopamine than the controls. I found no studies that gave mice an injection of Uridine on one day and then on same day provoked a release of dopamine. My guess would be that the release of dopamine would be the same or even LESS than controls based on my nightmare experience with it. But maybe, just maybe, choline and uridine taken every morning for month after month (like magnesium, might) will increase our receptors as it does the mice and give us some relief. And if you stop the choline and uridine, then eventually your receptors will shrink again because we don't have any frickin iron to keep them robust. I would imagine that drug addicts who take these substances can probably stop after a few months and their once shrunkin (due to drug abuse) now bigger stronger receptors will stay that way because that is baseline receptors for drug addicts. Only we're not drug addicts, and our baseline receptors are pretty pathetic. So like those iron infusions that have to be repeated (which I believe shore up our receptors if the right kind of iron is infused) any extended treatment with choline and uridine would probably have to be repeated as our bigger better receptors start to return to baseline as they do with the iron infusions.

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