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Re: 2nd Q on paradoxical stim. response - z, anybody?

Posted by King Vultan on August 27, 2004, at 12:37:13

In reply to 2nd Q on paradoxical stim. response - z, anybody?, posted by KaraS on August 26, 2004, at 20:16:29

> Here's an article that talks about neuroreceptor malfunction in those with CFS as a cause of their paradoxical stimulant response. (Please don't move this post Dr. Bob because my question isn't about CFS, but rather about stimulants, neuroreceptors and paradoxical response.)
> Anyhow, I had a few questions on it but wanted to post it first for reaction and to see if it made sense to others out there. Do you think it's consistently saying the same thing?

If what he is saying is true, and I have good reason to believe there is at least some truth to it, it provides some insight into what very well could be my fundamental problem. I'm familiar with the concept of hypersensitive presynaptic 5-HT autoreceptors, as this is an important part of the theory of how SSRIs work, but I guess I had never stopped to consider that dopamine autoreceptors might be hypersensitive also.

My experience with true stimulants is limited, as I've only tried Provigil in the stimulant class. The mechanism by which this drug works is not completely understood, but one of the end results is thought to be an increase in the availability of dopamine. In my case, I found Provigil to be the most profoundly sedating drug I've ever tried, and if his hypothesis is correct, it implies I have too many dopamine autoreceptors, which is the essence of hypersensitivity. However, to my way of thinking, it should be possible to get those receptors to downregulate by bombarding them with dopamine in the same way that SSRIs downregulate 5-HT1A presynaptic autoreceptors with the extra serotonin made available by blocking reuptake. I would think that either a dopamine reuptake inhibitor (Wellbutrin), a stimulant (Ritalin, amphetamines, etc.), or an MAOI with stimulant properties (Parnate, selegiline) acting for a long enough period of time should cause the dopamine autoreceptors to downregulate such that the neuron can resume normal firing. However, it's probably not that simple in practice.





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