Posted by KarenRB53 on April 15, 2008, at 12:43:58
In reply to Re: Inderal-vs-Pindolol » SLS, posted by JohnX on April 16, 2001, at 3:05:17
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> > > > Both pindolol (Visken) and propanolol (Inderal) antagonize (block) NE beta receptors. It is this action that is responsible for their therapeutic effects in cardiovasculature conditions. However, the property of pindolol that is thought to be most involved in its proposed antidepressant action is the antagonism of serotonergic 5-HT alpha-1a autoreceptors, a receptor that is not affected by propanolol. The antagonism of these autoreceptors actually increases the sensitivity and firing rate of serotonergic neurons. The two drugs are best not thought of as being interchangeable when used for depressions.
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> > > Propranolol from what I have seen also has an antagonist effect on the serotonin 5ht-1a receptor. However, it has not been shown to have much of an anti-depressant benefit. Many markers of anti-depressant action are down-regulation of beta-adrenoreceptor. Propranolol being a full beta blocker actually has a potential side effect of inducing depression as it potently blocks the beta-adrenoreceptor. Pindolol is a partial antagonist (or agonist, which ever way you look at it). So I suspect this is part of the reason that it does not induce depression and the 5ht action is anti-depressant. Any thoughts?
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> > Thanks for the correction, John.
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> > I was surprised to see propanolol listed as a 5-HT1a antagonist, as I have not seen this mentioned in the literature I have come across. Pindolol seems to be the drug more often chosen as the probe in experiments. When I looked specifically for studies for which propanolol was used, it seemed to be considered as being very close to pindolol in potency.
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> > You are quite a bit more familiar with the relative actions of these drugs on NE beta receptors than am I. A possibly important consideration in comparing the antidepressant effects of pindolol versus propanolol is that pindolol seems to show a higher affinity as an antagonist of presynaptic 5-HT1b autoreceptors. This action would act synergistically with its 5-HT1a antagonism to promote an increase in serotonergic neurotransmission. Perhaps, as you have stated, pindolol is only a partial antagonist at NE beta receptors, it might be less depressogenic than propanolol (I believe that notion that propanolol is depressogenic is still a point of debate). Thus, it is conceivable that the antidepressant effects of pindolol mediated through 5-HT1a/b antagonism predominate over a reduced depressogenic potential. Conversely, the relative lack of 5-HT1b antagonism by propanolol, coupled with its more potent NE beta antagonism, yields a net neutral or depressogenic result.
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> > Thanks for motivating me to look into it. The thoughts I offered here seem too simplistic to me, and something seems to be missing. Ill let you fill in the blanks.
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> > :-)
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> > - Scott
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> Hi Scott,
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> I'm not an expert on these beta-blockers by any means, I just know what I experienced on Inderal and information given to me by a Neurologist. This spurred me to try to better understand the actions of Inderal. Seems it is better used as an anti-anxiety agent. It has been studied for the use of bruxism as well as other ailments like tension headaches. It worked for me but the neurologist took me off of it because he was afraid it could exacerbate my depression (it is listed as a potential side effect).
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> In a chapter on treatment for neuroleptic induced EPS in the American Psychiatric Press textbook of Psychopharmacology, beta-blockers like Inderal were listed as being very effective in treating symptoms such as akathasia . Thus they are sometimes helpful in the use of RLS.
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> I'm not an expert on the mode of action, but I think it may have more to do with the 5ht-1a action somehow inhibiting serotonergic firing of the raphe extensions than anything the beta-blockade does (You probably know more than me about the specifics of 5ht-1 modulation). The raphe extensions modulate dopamine firing into the prefrontal cortex (where the neuronal control of masticatory muscles are). A hypodopaminergic prefrontal cortex can cause facial muscular contractions. Hypodopaminergic states can also cause akathasia (feelings of restlessness as in RLS). My experience is that beta-blockers,dopaminergic meds,and 5ht-2 antagonists releave my tension headaches. 5ht-2 antagonism will also relieve hypodopaminergic prefrontal cortex state. I believe that my treatment by SSRI's may have induced my chronic problems since they triggered them very badly when I took them.
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> My reactions to anti-depressants was quite bizarre. When I took ADs that worked like Zoloft, they usually induced a short lived manic state followed by a sporadic switch into a completely emotionless state with massive muscle contraction in my face. I found an article about SSRI induced tension headaches (specifically pointed the finger at Zoloft) and it talked about the raphe serotonergic modulation of mesocortical dopamine firing and suggested treating the headaches with buspar (or a 5ht-2 antagonist).
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> I would almost call my reaction to the ADs as a "schizophrenic" like switch from positive to negative psychosis. Negative psychosis is characterized by emotional numbing and is believed from my research to be related to hypodopamergic (pre)frontal cortex. That's why 5ht-2 antagonism in the atypical anti-psychotics better relieve the negative aspects of schizophrenia. I also believe that the 5ht-2 antagonism in meds like zyprexa relieve anhedonia,dysthymia and other sometimes difficult to treat depression symptoms. Just my hypothesis....
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> any follow up thoughts?
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> -John
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This is such an old posting I don't know if you'll get it or not. My question is ...Prozac works best for my depression however because I have essential tremor it does cause the tremor to worsen at times and also the Prozac does nothing to help my anxiety. In your opinion, would you think I should try Propranolol or Pindolol? Thanks for any advice.Karen
poster:KarenRB53
thread:59717
URL: http://www.dr-bob.org/babble/20080412/msgs/823442.html