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diacetyl-dopamine

wungchow

wungchow

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Would acetylating dopamine allow it to penetrate the CNS (in a manner similar to heroin?) Basically I'm wondering if the ester link is hydrolyzed before or after CNS penetration.
 
Link I would hazard a guess that 'yes' is the answer. Doesn't L-DOPA have rather nasty side-effects?
 
Hahaha I was just thinking about this same thing and how happily it turns out somebody has already made a thread like this... Yeah, acetylating dopamine should make it cross the BBB which could yield in a very euphoric effect of pure dopamine! Or it could work like a dopaminergic like L-DOPA. It is hard to tell. You would have to snort the diacetyl-dopamine though so that it bypasses liver deacetylation and deacetylates in the brain. And it would actually probably be more effective then the benzoyldopamine since it acetyl is still about just as polar and hydrolyzes 100 times better to dopamine while inside.

And the interesting thing is that even if diacetyldopamine isn't much fun, you could acetylate anything! Ephedrine doesn't have much effects because of the polar-OH meaning it can't cross BBB. But some acetic anhydride and it should be as potent as amphetamine! Or you can crank your brain up and acetylate epinephrine so it can get into CNS and make you super alert. And the nice thing is- all you need is acetic anhydride. Wungchow you're a smart man.
 
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sorry to piss on your fireworks, but

1, how long to expect diacetyl dopamine to survive hydrolysis by plasma esterases? the half life is going to be measured in minutes, if not seconds.

2, dopamine has an amino group also, which can form an acetamide.

3 why do people think that DA or a non selective DA mimic is going to be any fun at all?
 
People think that

drug x releases dopamine
drug x feels goooood
therefore dopamine feels goooood

which however is not the case. Dopamine is a neurotransmitter. Not a feel-good-drug. It plays a part in transmitting signals across the neurons, thus creating the thought process in your head. Increasing the amount of dopamine does not necessarily amount to euphoria, or stimulation.
 
dread said:
People think that

drug x releases dopamine
drug x feels goooood
therefore dopamine feels goooood

which however is not the case. Dopamine is a neurotransmitter. Not a feel-good-drug. It plays a part in transmitting signals across the neurons, thus creating the thought process in your head. Increasing the amount of dopamine does not necessarily amount to euphoria, or stimulation.
Click to expand...

yea, its more related to timing and flooding the brain. We feel the euphoria because they dopamine sharply rises and floods the brain. I've heard LDOPA dosen't do much though as far as euphoria and has shitty sides.

There are people I've talked to that say L-tyrosine works good for energy and depression.


P.S. - wung, is that a porn star in your avatar? looks familiar
 
Assume for a moment that this does facilitate BBB diffusion. What would be the rate limiting step if decarboxylase is bypassed? Wouldn't central dopamine bombardment precipitate neuronal apoptosis?

Does anyone know of any murine studies involving intraventricular DA?

By the way, l-dopa is great for wood.
 
seep said:
Assume for a moment that this does facilitate BBB diffusion. What would be the rate limiting step if decarboxylase is bypassed? Wouldn't central dopamine bombardment precipitate neuronal apoptosis?
Click to expand...

There only rate limiting step is the deacetylation which is quite rapid, similar to heroin. It would have to be snorted though to avoid liver deacetylation, and perhaps MAO in the intestine.

Thing is though it probably won't be that euphoric. Probably just like dopamine agonists (i.e. pramipexole). But if you have some dopamine and some acetic anhydride, by all means.
 
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mmm...classic direct d2 agonists tend to make people spew rather than feel euphoric (although the latter is an 'occasional' side-effect).

I'm pretty sure that we're barking up the wrong tree.

ebola
 
Hahaha you're right it probably wouldn't do anything but it is interesting, it is dopamine right? Plus full receptor agonism D1-D4 (although I suppose so is L-Dopa)... well it's interesting anyways.
 
PetersKeys said:
yea, its more related to timing and flooding the brain. We feel the euphoria because they dopamine sharply rises and floods the brain. I've heard LDOPA dosen't do much though as far as euphoria and has shitty sides.

There are people I've talked to that say L-tyrosine works good for energy and depression.


P.S. - wung, is that a porn star in your avatar? looks familiar
Click to expand...

Actually, that isn't the case either.
 
I think it's because if you use l-dopa you simply increase the amount of dopamine that's produced, but this doesn't necessarily mean it's released any more than without it and as such it's not flooding the receptors with dopamine at all like with stimulants.
 
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If Haribo was around, he'd note that Barry Kidston (sp?) apparently abused his L-dopa.
 
I thought he got Parkinson's from his opiate experiments MPTP, so he had to take L-dopa afterwards...

During the seventies, a student living in Massachussetts by the name of Barry Kidston became curious about hard drugs, and wanted to experiment with them. Being a chemistry major, Barry decided to synthesize the drugs himself rather than put himself at risk by traveling to bad neighborhoods to purchase them. Barry became particularly interested in a synthetic analog of Demerol known as MPPP.

Barry set up a laboratory in the basement of his parents' home, and was able to synthesize and use MPPP for several months without incident. However, on one occasion he was forced to hurry through the steps of manufacture for a batch of MPPP, and something went wrong in the process. When Barry injected the product, it produced a pronounced unexpected burning sensation, and three days later, he began to experience bradykinesia (a severe slowing of movements) severe enough that he had to be admitted to a hospital. After unsuccessful attempts to treat him with neuroleptics, a neurologist diagnosed Parkinson's disease, and he was put on L-Dopa, which improved his symptoms.

The National Institute of Health was notified about this rare case, and a team was sent to Kidston's home to investigate the etiology of his condition. Fortunately, some of the poisonously mis-synthesized drug was still present in the glassware he had used to cook it, and the NIH decided to perform testing on two of the compounds they found: MPPP, and MPTP, an unexpected by-product.

These compounds were tested in rats, and MPTP did cause the rodents to exhibit Parkinsonian-like symptoms for a few hours. However, the researchers were unable to reproduce the permanent condition that afflicted Barry. This was unfortunately just a case of bad luck. Later research has shown that rats are specifically resistant to the toxic effects of MPTP.

In 1982, six young people in the Bay Area of California suddenly manifested a Parkinson-like syndrome. Doctors were baffled by these cases - the patients were too young, and the symptoms manifested too abruptly to be true Parkinson's disease. It was later determined that these patients were all addicts that had taken a synthetic heroin then going by the name of "China White", which a local drug dealer had been manufacturing in his garage. This turned out to be - you guessed it - a MPTP-contaminated batch of MPPP.

From these two separate incidents, scientists were able to determine that MPTP was the responsible agent. Studying of the action of MPTP on the brain, scientists determined that the action of MPTP's metabolite MPP+ is very similar in effect to that of paraquat, a pesticide, which has led to the investigation of pesticides and other environmental factors as influences in the development of Parkinson's disease. It was eventually discovered that MPTP causes Parkinsonianism in primates, and the syndrome is frequently studied in these creatures as an animal model of the human disease.
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I would not be afraid to try certain untested compounds such as

3,4-dichloromethamphetamine or
3,4,5-trichloroamphetamine,

but the thought of IV (and that's about the only way I see to take this one)
3,4-di-acetyl-dopamine scares even me.
 
I still think that this compound would be worth exploring. Dopamine is a full dopamine agonist (D1,D2,D3,D4) and this is what I found about D1 agonists:

"D1-selective full agonists like SKF-81297 and 6-Br-APB produce characteristic anorectic effects, hyperactivity and self-administration in animals, with a similar but not identical profile to that of dopaminergic stimulants such as amphetamine"

Dopamine would also probably be somewhat like pramipexole with the D2/D3 agonism.

Say the diacetyl-dopamine does cross the BBB and gets deacetylated (I think a good bit of it should), I would think the dopamine should just be able to flood over the receptors (although it probably won't last long due to MAO, COMT, DAT).
 
Yeah, he needed levodopa to treat his symptoms, but he abused it and as such, it was discontinued (or continued with some strings, maybe, i guess)
 
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