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Don't know what this says


kim

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First, I need a better understanding of tyrosine hydroxlase. I want to know how infection/virus can affect dopamine expression, I'm just going to do this a little at a time, in case there is anything here that helps. I usually end up with a bunch of links and excerpts on a note pad, and can't explain what I found, anyway, so I'm just going to try here.

 

Here, we show that human Tregs constitutively express tyrosine hydroxylase (TH, EC 1.14.16.2 [EC] )

 

From http://en.wikipedia.org/wiki/Tyrosine_hydroxylase

 

Tyrosine hydroxylase or tyrosine 3-monooxygenase is the enzyme responsible for catalyzing the conversion of the amino acid L-tyrosine to dihydroxyphenylalanine (DOPA). DOPA is a precursor for dopamine which in turn is a precursor for norepinephrine (noradrenaline) and epinephrine (adrenaline).

 

The enzyme, an oxygenase, is found in the cytosol of all cells containing catecholamines. This initial reaction is the rate limiting step in the production of catecholamines

Here, we show that human Tregs constitutively express tyrosine hydroxylase (TH, EC 1.14.16.2 [EC] ), the rate-limiting enzyme in the synthesis of catecholamines, and contain substantial amounts of dopamine, norepinephrine, and epinephrine, which are released upon treatment with reserpine.

 

So what is Reserpine?

 

http://en.wikipedia.org/wiki/Reserpine

 

Reserpine was isolated in 1952 from the dried root of Rauwolfia serpentina (Indian snakeroot),[5](which had been known as Sarpaganda and had been used for centuries there for the treatment of insanity, as well as fever and snakebites[2]) and introduced it in 1954, two years after chlorpromazine.[6] Reserpine almost irreversibly blocks the uptake (and storage) of norepinephrine (i.e. noradrenaline) and dopamine into synaptic vesicles by inhibiting the Vesicular Monoamine Transporters (VMAT).[7]

 

and

 

Reserpine is an indole alkaloid[3]antipsychotic and antihypertensive drug that has been used for the control of high blood pressure and for the relief of psychotic behaviors, although because of the development of better drugs for these purposes and because of its numerous side-effects, it is rarely used today.[1] Reserpine is acts via the disruption of norepinepherine, serotonin, and dopamine presynaptic vesicles. The neurotransmitters are subsequently metabolized by MAO and therefore never reach the synapse

 

The antihypertensive actions of Reserpine are a result of its ability to deplete catecholamines (amoung the others) from peripheral sympathetic nerve endings. These substances are normally involved in controlling heart rate, force of cardiac contraction and peripheral resistance. .[4]Reserpine depletion of monoamine neurotransmitters in the synapses is often cited as evidence to the theory that depletion of the neurotransmitters causes subsequent depression in humans. Moreover, reserpine has a peripheral action in many parts of the body, resulting in a preponderance of the cholinergic part of the nervous system (GI-Tract, smooth muscles vessels).
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