Posted by schleprock on December 27, 2012, at 18:54:42
In reply to Re: feel finished » schleprock, posted by SLS on December 27, 2012, at 14:18:03
> Hi schleprock.
>
> > SLS, Could you please provide details on your experience with Prazosin? specifically it's effect on your depression and its suspected mechanism of action. I looked it up and noticed it was an alpha blocker. I was previously on beta blockers (atenolol and propranolol) and am thinking of going back to one (if I fail to have any progress with Buspar.) What are the advantages in choosing an alpha blocker over a beta-blocker?
>
> First of all, it is important to note that I was taking 5 other drugs before adding the prazosin. However, in studies of PTSD, prazosin monotherapy produced improvements in anxiety and depression. For me, prazosin feels like a very clean, robust, and broad-spectrum antidepressant. It reduces the severity of the entire scope of depressive symptoms. The one exception to this is sexual libido. Reduced libido is a side effect of prazosin, and it showed up immediately. However, the resolution of depression helps to offset this, as depression pretty much wiped-out my sex-drive to begin with.
>
> NE alpha receptors and NE beta receptors are not interchangeable. Although they can both function as sympatholytics, they are not evenly distributed in the brain, and serve different circuits. Although three subtypes of receptor exist, my guess is that it is the NE alpha-1b receptors that are critical in modulating mood. Prazosin is more potent here than are other NE alpha receptor antagonists.
>
> I am playing with the idea that blocking these receptors in the brain structure known as Brodmanns Area 25 produces antidepressant effects similar to deep brain stimulation (DBS), which seems to work by interfering (reducing) neurotransmission there. In addition, NE alpha-1b receptors exist in the amygdala, an area known to be responsible for producing fear and anxiety. They also exist in the nucleus accumbens, where they seem to antagonize incoming glutamatergic circuits. This would most likely result in an increase in dopaminergic activity there via disinhibition. There really isn't very much research into the pharmacological actions of prazosin to reduce PTSD and depression. I am left to offer only a lot of guesses.
>
> Prazosin - NE alpha-1a/b/d receptor antagonist.
>
> 1. Reduce hyperactivity in Brodmann Area 25 (anterior subgenual cingulate).
>
> 2. Reduce hyperactivity in amygdala.
>
> 3. Increase dopaminergic activity in the nucleus accumbens.
>
> You might want to check out the following thread. It is rather long, but might be worth a look. Here is a relevant post:
>
> http://www.dr-bob.org/babble/20120202/msgs/1009565.html
>
> To be honest with you, I haven't researched this thing very much. Nowadays, I am interested in doing the minimum amount of research that will facilitate my getting well.
>
>
> - ScottThanks SLS. Found this article:
http://www.ehow.com/facts_5695241_alpha-blocker-vs_-beta-blocker.html
So basically one class lowers norepinephrine while one lowers epinephrine. The article manages to make the side-effects of Alphas sound much worse than Betas. Atenolol (not over 12.5 mg) I know I've been able to tolerate. Not sure what to do...
Do you also believe bet blockers to be an effective adjunct treatment for anxiety\depression, or only alpha blockers?
poster:schleprock
thread:1033817
URL: http://www.dr-bob.org/babble/20121217/msgs/1034001.html