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Re: 'Prozac not potent (...)' - Yes it is!

Posted by Franz on April 2, 2011, at 18:09:29

In reply to Re: 'Prozac not potent (...)' - Yes it is!, posted by Brainbeard on December 30, 2009, at 13:45:29

> The idea that Prozac (i.e. fluoxetine) would not be a potent 5HT2c-antagonist is based on a misunderstanding. The Ki values are misleading, because serotonin reuptake inhibition and 5HT2C-antagonism cannot be compared equally. Serotonin receptors have to be (nearly) saturated by a reuptake blocking molecule for SRI to reach clinical significance. 5HT2C receptors, on the other hand, only need a little antagonism to result in significant effects (boosted dopamine and noradrenaline, basically). So you can't compare the Ki values on an equal par at all.
>
> The most informative study on the difference between the two mechanisms that I could find on the web is this: http://www.pnas.org/content/94/5/2036.full.pdf
>
> A quote: 'So far, the therapeutic effects of fluoxetine have been attributed primarily to its inhibition of 5HT transporters. Interestingly, it has been shown that the therapeutic plasma concentration of fluoxetine is in the micromolar range, and our studies show that, at this concentration range, fluoxetine can potently inhibit the membrane current responses mediated by 5HT2C receptors. Moreover, the affinity of fluoxetine for 5HT2C receptors (Ki 5 65 nM) is close to its affinity for 5HT transporters (Ki 5 33 nM) (29), which is also well below the therapeutic plasma concentration of fluoxetine. Thus, some therapeutic effects of fluoxetine may be a consequence of blocking both 5HT transporters and 5HT2C receptors. It should be noted that the blockage of 5HT transporters and that of 5HT2C receptors would have opposing actions on serotonergic synaptic transmission. (.....) Because of the highly nonlinear dose/response relationship of 5HT2C receptors the blockage of even a small number of receptors in a cell would lead to very profound changes (.....)'.
>
> Interestingly, the Ki value for agomelatine's binding to the 5HT2C receptor is way higher than Prozac's: it's 710nM! (http://www.medicographia.com/html/static/html/issues/article_latest.asp?page=issues/99/art_10/p_2) So you reached your conclusion that agomelatine is a better option a bit too fast. This proves my point that only a little binding to 5HT2C receptors yields a clinically significant effect.
>
> So Prozac IS a potent 5HT2C-antagonist, and at lower doses this IS the main mechanism behind its effectiveness as an antidepressant.

What would be a low dose prozac with 5HT2C-antagonist effect?

How bad is prozac´s effect on sexual function for males?

I am considering alternatives to agomelatine.

Thanks

 

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Psycho-Babble Neurotransmitters | Framed

poster:Franz thread:927037
URL: http://www.dr-bob.org/babble/neuro/20100607/msgs/981763.html