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Re: DA downregulation Postsynaptic Hypothesis. dazednconfused

Posted by JohnX2 on February 16, 2002, at 11:52:33

In reply to DA downregulation Postsynaptic Hypothesis., posted by dazednconfused on February 16, 2002, at 10:25:15

I have a DA upregulation theory.
I believe there is a theory that the brain can developed something
called "reverse tolerance". This can occur when someone
abuses stimulants. The brain pops up many post synaptic
dopamine d2 receptors to compensate for the enormous amounts
of dopamine being constantly pounded into the synapse. The same
d2 postsynaptic receptors that make you feel good also tell
the presynaptic receptor to stop sending dopamine. So after
a while you need to take A LOT more of the medicine in order
to get the medicine to work because of this enhanced feedback.
This is just a theory.
I think it may hold true for a reuptake inhibitor also.
The reuptake inhibitor leaves more dopamine in the synapes
and it occupies the posnaptic d2 receptors which in turn
feedback to tell the presynaptic receptor to stop sendind
dopamine and you wind up with less dopamine not more.
I could be wrong here and someone can correct me.


> 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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