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/16923332So 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.