Does anyone know if it is possible to modify Dopamine HCl so it can be passed through the blood vessel brain barrier to allow it to reach neurons?

Yes, methylate the -OH groups on the aromatic ring. However the result will not be dopamine and thus it is impossible.

I think an intercerebrospinal injection of dopamine is what you want  

Methylating it will not help much, since 3,4-dimethoxyphenethylamine is completely inactive. I think this molecule is decomposed quickly by the body's MAO enzymes.

You can always try to brominate the latter though, it could be that 2-bromo-4,5-dimethoxyphenethylamine has some activity. We will not know until someone tries it out.

Or you could use the dopamine to inject Trichocereus cacti, as these will biosynthesize mescaline from it.

Di-O-acetylation should do the trick. Alpha-methylation would help against premature degradation.

But still wouldn't it be better to use injection as route of administration, certainly for the PEA and maybe also for the amphetamine?

I can probably assume that the di-O-acetyl analogs will not be more potent than 3,4-DMPEA/3,4-DMA ?

3,4-DMA should be a bit weaker than mescaline (observed logMU = -0.06, about equipotent as mescaline), while 3,4-DMPEA is quite a bit weaker (logMU = -0.67)

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I think this molecule is decomposed quickly by the body's MAO enzymes.

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L-Deprenyl would fix that.

Seliginine (l-deprenyl) is a MAO-B inhibitor, like eg. yohimbine also is. For this purpose you'd need a MAO-A inhibitor, such as harmaline or a non-selective one like iproniazide. I would strongly recommend against doing such a thing, however.

Do you have a reference that yohimbine is any type of MAOI?

Also, MAO-B preferentially deaminates dopamine and phenethylamine. If this DA analogue is subject to oxidative deamination by MAO it would be MAO-B, not MAO-A. MAO-A preferentially deaminates norepinephrine, tyramine and tryptamines and is primarily found in the peripheary.

When searching for the article that claimed this a while ago, I stumbled on this one:

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However, we haven't seen any conclusive study on yohimbe and MAO inhibition. If yohimbe were a strong and definite MAO inhibitor, one would have to expect fatalities if the usual precautions against tyramine-containing foods were not heeded. Any herb that functioned as a definite MAO inhibitor would long ago have been classified as a poison. But yohimbe has been sold as a supplement for years. If incidences of death would have occurred after ingesting yohimbe because of yohimbe being a MAO inhibitor, it's unlikely this fact would not be reported widely. Alas, there are no widely circulating reports of yohimbe causing deaths because of its effects as MAO inhibitor.

http://www.yohimbe.org/chairmanmao.htm

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Have there been any known trials with MAO-B inhibitors and dopamine or phenethylamine yet? It should be very interesting, but still I'd proceed with extreme care, starting with very low doses first.

Vitus: The acetylated compound would be quickly desacetylated. If this happens after passing the BBB we have won    We could fine-tuni the desacetylation-halflife by using other (i.e. longer or branched) esters.

Well trials with MAOIs and DA would be useless, DA cannot cross the BBB. There have been limited trials w/ L-Deprenyl in combination with phenethylamine and L-Deprenyl with phenylalanine.

3-hydroxy-L-tyrosine crosses the BBB and is promptly decarboxylated into dopamine.

It is used in the treatment of Parkinsonism along with carbidopa (a peripheral inhibitor of decarboxylation -- so the dopa isn't converted outside of the brain), and entacapone (an inhibitor of a step in dopamine breakdown).