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DA downregulation Postsynaptic Hypothesis.

Posted by dazednconfused on February 16, 2002, at 10:25:15

Hi to everybody interested or not in this stuff.
I've read an interesting theory about inefficency of some dopaminergics meds used in dopaminergic deficency in the brain (distymie, aphatie, anaergie.....)and i'll show it to you:
The Classic theory says that negative sympthoms are generated by the poor quantity of dopamine in the intercellular zones of the brain, so, the postsynaptic receptors are not able to catch it and make it be available for the brain-cell (neurons).
So, if you use a dopaminergic med (amisulpride, bupropione, pramipexole...) you'll increase the quantity of dopamine in the intercellular space and, consequently, the postsynaptic receptor can use more dopamine for the cells.
This theory, however, can't explain why the dopaminergic meds are effective in less than 50 p.c. of dopaminergic lack, more than 50 p.c. do not have improvement in using this meds (i'm one of them).
The new theory i have read do not contradict classic one, but it try to expain why 50 p.c. of cases don't have improvement in the more dopamine quantity present in the brain after the use of dopaminergic meds:
It says that in some cases the lack of dopamine in the brain is not caused by the "lack of total quantity" but by the "lack of postsynaptic receptors" in the various zones of the brain.
So you can increase the quantity of dopamine as you like, more and more, but it can't anyway be used by your neurons, cause you do not have enough receptors to catch and to use it!
So, what should we do in this case?
I've not read anything about it!
But i think that you must increase the permeability of your cellular skin (SAME, Sodium Valporate?) or try to remodulate your neurotrasmetiptorial system acting on other like Serotonine, that seems to control even on dopaminergic one.
But these are only suppositions!
Bye


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poster:dazednconfused thread:94402
URL: http://www.dr-bob.org/babble/20020215/msgs/94402.html