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Dr. Bob is Robert Hsiung, MD,
bob@dr-bob.orgShown: posts 1 to 4 of 4. This is the beginning of the thread.
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
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.-John
> 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
Posted by dazednconfused on February 18, 2002, at 7:17:10
In reply to Re: DA downregulation Postsynaptic Hypothesis. » dazednconfused, posted by JohnX2 on February 16, 2002, at 11:52:33
Hi John,
your theory is quite interesting!
If i had understand well you mean that:
more dopamine in the synaptic zone=more post-syn aptic receptors;
more post-synaptic receptors=more pre-synaptic receptors;
more pre-synaptic receptors=more reuptake of dopamine in the intercell zone;
more reuptake of dopamine=less dopamine available in your brain.
The circle is closed and it seems don't to have an end!
I could be agree with you, but let me suppose that we could break this circle:
we know that 100 mg of amisulpride, L-sulpiride or 400 mg of sulpiride, totally saturate the pre-synaptic receptor, making them completely off.
So we could stop the reuptake of dopamine at all!
However, if it shouldn't works, we could anyway increase the amount of dopaminergic med till we could block all pre-synaptic recetors.
You know you could increase amisulpride up to 400 mg or more without interact with post-synaptic cell, and so, acting only at pre-synaptic receptors level.
What's your opinion about? What could you suppose to do in this case?
Bye
Posted by JohnX2 on February 18, 2002, at 15:16:15
In reply to Re: DA downregulation Postsynaptic Hypothesis. » JohnX2, posted by dazednconfused on February 18, 2002, at 7:17:10
I need to think about your idea.
I haven't tried (ami)sulpride, but would like
to.Regards,
John> Hi John,
> your theory is quite interesting!
> If i had understand well you mean that:
> more dopamine in the synaptic zone=more post-syn aptic receptors;
> more post-synaptic receptors=more pre-synaptic receptors;
> more pre-synaptic receptors=more reuptake of dopamine in the intercell zone;
> more reuptake of dopamine=less dopamine available in your brain.
> The circle is closed and it seems don't to have an end!
> I could be agree with you, but let me suppose that we could break this circle:
> we know that 100 mg of amisulpride, L-sulpiride or 400 mg of sulpiride, totally saturate the pre-synaptic receptor, making them completely off.
> So we could stop the reuptake of dopamine at all!
> However, if it shouldn't works, we could anyway increase the amount of dopaminergic med till we could block all pre-synaptic recetors.
> You know you could increase amisulpride up to 400 mg or more without interact with post-synaptic cell, and so, acting only at pre-synaptic receptors level.
> What's your opinion about? What could you suppose to do in this case?
> Bye
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