Posted by SLS on January 4, 2012, at 5:55:26
In reply to Re: Adding Parnate and prazosin., posted by Bob on January 4, 2012, at 3:39:20
Hi Bob.
It was nice of you to notice my post. It might be an important observation that prazosin has produced such a significant improvement in my condition.
Just to let you know, I performed an experiment to verify that prazosin was the agent responsible for my improvement. I discontinued it for 36 hours and observed that I relapsed pretty hard. I was able to recapture the antidepressant response immediately upon the reintroducton of prazosin. Upon titration, I settled on 6 mg as the dosage. Hopefully, this is the dosage that will bring about a full remission. My instincts tell me that it will.
> OK, so in lay terms what does this mean?
Chronic (long-term) antidepressant treatment with certain drugs causes the norepinephrine NE alpha-1 receptors to downregulate by reducing their numbers. Prazosin blocks these same receptors, thereby producing the same net effect.
I am, of course, extremely interested in the way prazosin might work for others as it now works for me. (Please God, let it continue). Perhaps prazosin has been overlooked in the treatment of TRD.
For now, I would say that prazosin might work best as an adjunct to antidepressants for people who have a history of childhood physical abuse, emotional abuse (including bullying), or neglect. It may be that some people have a backdrop of PTSD acting to drive depression. Does pazosin also work for other subtypes of depression? I don't know.
- Scott
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> > This is an interesting abstract that reports a downregulation of NE alpha-1 (prazosin) binding with antidepressant use.
> >
> > -----------------------------------------
> >
> > J Neural Transm. 2010 Dec;117(12):1423-30. Epub 2010 Dec 7.
> >
> > Differential modulation of a-1 adrenoceptor subtypes by antidepressants in the rat brain.
> >
> > Ramakrishna D, Subhash MN.
> > Source
> >
> > Kamineni Institute of Medical Sciences, Sreepuram, Narketpally, Nalgonda 508254, Andhra Pradesh, India. drramakrishna@klsindia.com
> > Abstract
> >
> > The aim of the present study was to examine the effect of chronic antidepressants treatment on the density of a1-adrenoceptor (AR) subtypes in rat brain. Density of total a1 and a(1A)- and a(1?)-ARs was measured in cortex and cerebellum of rats treated with amitriptyline (AMI), desipramine (DMI) and fluoxetine (FLX), (10 mg/kg body wt), for 30 days, using [³H]prazosin in presence and absence of WB-4101. The density of cortical total a1-ARs was significantly decreased with AMI (54%) and DMI (25%) treatment, without altering the affinity of the receptor. Fluoxetine did not alter the density of cortical a1-ARs. The density of cortical a(1A)-ARs was also significantly decreased with AMI (85%) and DMI (50%) treatment, without affecting the affinity. The density of cerebellar total a1-ARs was significantly decreased with AMI (37%), DMI (50%) and FLX (70%) treatment, without affecting the affinity for [³H]prazosin. The density of a(1A)-ARs was significantly decreased with AMI (67%), DMI (59%) and FLX (92%) treatment. a(1B)-AR density was decreased only with FLX (47%) and DMI (47%) treatment. Correspondingly the basal IP3 and NE (10 µM) stimulated IP3 levels were significantly decreased in AMI (47%), DMI (22%) and FLX (48%) treated rat cortex. The results suggest that chronic antidepressant (AD) treatment down-regulates the cortical and cerebellar total a1-ARs in rat brain. However, a(1A) subtype is predominantly down-regulated by AMI and DMI, where as FLX affects cerebellar a(1A)-ARs. The region-specific and subtype specific down-regulation of a1-ARs density, which occurs after prolonged AD treatment, may underline the therapeutic mechanism of action.
> >
> > PMID:
> > 21136124
> > [PubMed - indexed for MEDLINE]
Some see things as they are and ask why.
I dream of things that never were and ask why not.- George Bernard Shaw
poster:SLS
thread:1005781
URL: http://www.dr-bob.org/babble/20111226/msgs/1006288.html