LONGECITY

I've seen quite a few statements in this forum that high acetylcholine would lower dopamine. But when I was researching, all I could come up with was that higher acetylcholine levels would increase dopamine.
But if acetylcholine lowers dopamine, higher dopamine levels should lower acetylcholine. This would mean that serotonin would increase acetylcholine, since it decreases dopamine.
I can say from my own experience however, that high serotonin levels do produce symptoms of low acetylcholine (memory problems). But we know that dopamine and acetylcholine are important for memory.

So I am a bit confused. Whats the real relationship between dopamine and acetylcholine levels?

This is something I've been thinking about lately as well but the information about the matter is a bit confusing and too scattered. Definately would like to know the relationship between them etc. Anecdotally, my experience indicates that when dopamine is high, acetycholine is low and vice versa (obviously).

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I know from my own research that some choline rich foods such as eggs are said to be anti dopamine, is this from the food itself or from the higher choline?

A difference should be noted : high acetylcholine causes low dopamine concentration however as a consequence high acetylcholine causes high dopamine receptor binding (because more receptors are created when a molecule is depleted)
High acetylcholine increases serotonin and lowers dopamine, btw CDP choline upregulates D2.

what if we had methylphenidate, so that concentration of dapamine remains there???

Hmm. Then in theory, acetylcholine reuptake inhibitors such as donepezil should lower dopamine.

But they don't. At least not in the first 3 months.

http://www.ncbi.nlm....pubmed/20019232

Also:

We have also reported that methylphenidate (Ritalin®) induced behavioral activation consisting of increased talkativeness and interactions, as well as increased psychotic symptoms in psychotic patients, can be antagonized or prevented by administration of physostigmine (9). Similarly, methylphenidate-induced stereotyped
behavior in rats is decreased or prevented by physostigmine (10). Conversely, the anergic syndrome induced by physostigmine is readily reversed by injection of methylphenidate (9)...

physostigmine is an acetylcholine inhibitor. Less acetylcholine, less effect from ritalin, a dopamine reuptake inhibitor.
http://www.psychosom.../3/248.full.pdf

This sounds more like dopamine needs acetylcholine to work properly. And higher acetylcholine levels seem not to decrease dopamine? Vice versa it should be the same then.
Edited by BioFreak, 01 March 2013 - 08:18 PM.

According to Wikipedia, physostigmine is a reversible cholinesterase inhibitor, not an acetylcholine inhibitor.

You're right. thanks for pointing that out...

So more acetylcholine = less of a dopamine effect? Hmmm...

From a symptom perspective that would make sense... dopamine seems to make people more egoistic, while acetylcholine seems to make people more selfless.

Could it be that acetylcholine and dopamine do not affect each others levels but each others function?

Would there be any difference depending on the choline source, such as Alpha-GPC or Choline Bitrate?
Edited by Kyle McGill, 02 March 2013 - 04:41 AM.

I believe alpha gpc can cross the bbb direcly, while choline bitartrate needs to be reduced to choline so it can be transported via a choline transporter into the brain. Meaning less of an effect if you have no control over the effectiveness of the cholin transporter.

So you could use that to your advantage.

I'm right now experimenting with increasing acetylcholine through precursors ALCAR + CDP Choline and lecithin. So far I like the effects, esp the one of cdp.

I believe alpha gpc can cross the bbb direcly, while choline bitartrate needs to be reduced to choline so it can be transported via a choline transporter into the brain. Meaning less of an effect if you have no control over the effectiveness of the cholin transporter.

So you could use that to your advantage.

I'm right now experimenting with increasing acetylcholine through precursors ALCAR + CDP Choline and lecithin. So far I like the effects, esp the one of cdp.

what do you get more from cdp choline that you don't get from lecithin?

If higher acetylcholine levels decrease dopamine activity, then what about substances like piracetam which (supposedly) increases choline uptake without increasing choline level?


Is it the activity of the choline that matters or is it the amount of choline in the brain? Or are those two practically synonymous?

what do you get more from cdp choline that you don't get from lecithin?

cdp choline increases uridine levels in the brain, could increase dopamine receptor density I think.
Keep in mind that for choline to reach the brain it needs to use a transporter so it can cross the bbb, it can not do it directly which means that choline content in the brain is limited by choline transporters capacity. So you can artificially increase cholin content in the brain if the transporter is at its limit.

If higher acetylcholine levels decrease dopamine activity, then what about substances like piracetam which (supposedly) increases choline uptake without increasing choline level?

Is it the activity of the choline that matters or is it the amount of choline in the brain? Or are those two practically synonymous?

I think choline has different purposes in the brain, its part of the cell, and it can be used as precursor to acetylcholine.

What I know though is that the idea to lower acetylcholine or choline in an attempt to increase dopamine's effects is not a good idea.
For one, memory will get shitty. And I believe its about balance of dopamine and acetylcholine for both to work perfectly.

Our results showed that huperzine A (0.25, 0.5, and 0.75 micromol/kg, po) dose-dependently elevated extracellular acetylcholine (ACh) levels in the medial prefrontal cortex (mPFC) and hippocampus. Oral administration of donepezil (5.4 micromol/kg) or rivastigmine (1 micromol/kg) also elicited significant increases in ACh in the mPFC and hippocampus. The time course of cortical acetylcholinesterase (AChE) inhibition with the 3 inhibitors mirrored the increases of ACh at the same dose. The marked elevation of ACh after oral administration of huperzine A (0.5 micromol/kg) and donepezil (5.4 micromol/kg) was associated with a significantly increased release of dopamine (DA) in the mPFC or hippocampus. None of the 3 inhibitors affected norepinephrine (NE) and 5-hydroxytryptamine (5-HT) levels in the mPFC and hippocampus. The effects of huperzine A and rivastigmine did not depend on the route of administration, but donepezil was less efficacious by the oral route than by ip injection. The ability of huperzine A to increase ACh levels was unchanged when tests were performed after multiple oral administration of the drug at 0.5 micromol/kg, once per day for 30 d.

http://www.ncbi.nlm....pubmed/16923332

So increase acetylcholine, increase dopamine.

High-dose administration of psychostimulants traffics the vesicular monoamine transporter-2 (VMAT-2), as assessed by subcellular fractionation of rat striatal tissue. This study demonstrates that administration of low doses of amphetamine or methylphenidate differentially traffic VMAT-2 within nerve terminals, with effects similar to those observed after high-dose administration. Trafficking of vesicular glutamate, acetylcholine, or GABA transporters was not altered by high-or low-dose amphetamine or methylphenidate treatment. These data represent the first report that amphetamine redistributes VMAT-2 protein. In addition, these data demonstrate that the trafficking of VMAT-2 after amphetamine or methylphenidate is selective for monoaminergic neurons.

http://www.ncbi.nlm.nih.gov/pubmed/17618619

So an increase in acetylcholine does cause more dopamine to be released, while more dopamine does not release more acetylcholine. Interesting.
Edited by BioFreak, 05 March 2013 - 11:33 AM.

however if we elevate dopamine by inhibition of cholinesterase we will accelarate methylphenidate tolerance... Moreover this would have a negative effect on dopamine receptors?? making the evelation of acetylcholine useless....
i'm tire of thinking....

A difference should be noted : high acetylcholine causes low dopamine concentration however as a consequence high acetylcholine causes high dopamine receptor binding (because more receptors are created when a molecule is depleted)
High acetylcholine increases serotonin and lowers dopamine, btw CDP choline upregulates D2.

 High Ach doesn't increase serotonin. It decreases it. It also decreases dopamine.

 

Someone else above posted a study about  increased release of DA by high ach. That means less dopamine concentration in the brain, meaning it decreases it , it's depleted.

Edited by iseethelight, 11 October 2015 - 10:21 AM.

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high serotonin decreases acetylcholine and dopamine.