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Dopamine Metabolism Investigations

dopamine

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#1 abelard lindsay

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Posted 16 May 2015 - 01:15 AM


I've been looking at dopamine metabolism a bit and wanted to share some of my understanding.  I've bolded everything you can get readily as a supplement.

 

There's a nice diagram over at wikipedia that details the whole process of dopamine metabolism:

http://en.wikipedia....ical_mechanisms

 

Gets converted into PEA and Tyrosine.  PEA is the body's natural amphetamine that is quickly degraded by MAO-B and ALDH.

 

  • D-Phenylalanine - Synthetic D-isomer form of Phenylalanine

 Only gets converted into PEA 

 

  • Tyrosine - Found in many foods

 Gets converted into L-Dopa via Tyrosine Hydroxylase, the primary rate limiting enzyme in catecholamine metabolism.  

 

 Tyrosine Hydroxylase gets upregulated by nicotine and CREB activation (theoretically CILTEP)

 

  • L-Dopa - Intermediate Product, given as a drug to treat Parkinsons.  Also in Mucuna Pruriens.

 Vitamin B6 as P5P is a cofactor in the conversion of L-Dopa to Dopamine

 

  • Dopamine - Highly psychoactive compound associated largely with motivation

 Gets converted to norepinephrine. A cofactor in this conversion is Vitamin C.

 

 Dopamine can also get turned into DOPAL by MAO, which can lead to neurodegenerative consequences if the ALDH enzyme is not functioning.  This is more of a problem with leaky dopamine containing vesciles inside of neurons.  The diagram on this study is particularly helpful.

 

http://www.ncbi.nlm....pubmed/23786406

 

 

 

Determinants of buildup of the toxic dopamine metabolite DOPAL in Parkinson's disease.
Abstract

Intra-neuronal metabolism of dopamine (DA) begins with production of 3,4-dihydroxyphenylacetaldehyde (DOPAL),which is toxic. According to the 'catecholaldehyde hypothesis', DOPAL destroys nigrostriatal DA terminals and contributes to the profound putamen DA deficiency that characterizes Parkinson’s disease (PD).

...

Elevated DOPAL levels in PD putamen reflect a combination of decreased vesicular uptake of cytosolic DA and decreased DOPALdetoxification by ALDH.

 

 

More on methylation and dopamine next post...


Edited by abelard lindsay, 16 May 2015 - 01:23 AM.


#2 Mr Matsubayashi

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Posted 16 May 2015 - 03:55 AM

I'm interested in where this thread might lead. I haven't done any recent research but I just want to throw some ideas and questions out there.

 

Increased iodine intake increases dopamine. I believe part of the chain involves thyroxine.

There is a connection between dopamine and testosterone as well, I'm unsure which is the chicken and egg.

Poor sleep quality usually results in increased dopamine the following day. This might be an evolutionary trait to ensure proper functioning with a few days of poor rest.

There is a difference between tonic and phasic dopamine, is there an ideal ratio between the two for LTP?

Are there ways to create a offset with the autoreceptors such that higher tonic dopamine will not result in tolerance?

How does the consequences of dopamine excitotoxicity compare to serotonin or glutamate?

How much actual resilience to excitotoxicity is gained through BDNF, NGF, increasing agents?

I have read that excess tonic dopamine especially with a defect COMT can result in a toxic metabolic pathway, requires further research.

What are the required nutritional inputs for dopamine production and elimination.

Relationship between dopamine and CAMP.

How localised are the effects of dopamine in the brain? How localised are the effects of dopamine affecting drugs? Stimulant abuse and holes in the brain?

It's rare but some people can get by on very little sleep without performance issues, dopamine mutations might play a role.

Caffeine and tyrosine hydroxylase, caffeine causing a dopamine rush. Does theobromine (chocolate) have the same effect being a very similar molecule?

 

My personal interest in your research has to do with my COMT++ mutations. Characteristics which might result from this mutation based on my perception of myself vs others,

 

Sometimes my mind races but doesn't achieve much

I get great runners high

Stimulants have profound effects and then I crash. Cocoa powder and Modafinil both give me mania.

I have a high IQ but poor memory, it might be that my memory is in fact average but my high achieving cohort often exceed me.

I am relatively anxious

Winning gets me high

I tend to do things faster, talking, eating. When playing sport I accidentally give it my all even if the game is casual.


Edited by Mr Matsubayashi, 16 May 2015 - 03:58 AM.

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