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Re: ABILIFY may have trashed my LIBIDO » SLS

Posted by zeugma on February 8, 2005, at 17:24:17

In reply to Re: ABILIFY may have trashed my LIBIDO » zeugma, posted by SLS on February 5, 2005, at 6:13:00

Abilify seems to be helpful to me, and I would rather not have a reason to do without it. I am going to try, though, as an experiment. I'd like to see what happens to my libido and mood. I'll let you know.>>

Yes, please let me know. I am similarly trying the reverse: adding buspirone back in to my regimen. The main reason is because buspirone seems to have an antidepressant effect for me, though it is not a useful drug for most. So I took 15 mg am, plus I plan to take another 15 mg soon (with nortriptyline).

scott, what do you think of this report:

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=15363606

Prog Neuropsychopharmacol Biol Psychiatry. 2004 Aug;28(5):819-27. Related Articles, Links


Role of presynaptic alpha2-adrenoceptors in antidepressant action: recent findings from microdialysis studies.

Invernizzi RW, Garattini S.

Istituto di Ricerche Farmacologiche Mario Negri, Via Eritrea 62, 20157 Milano, Italy. rinvernizzi@marionegri.it

The therapeutic effect of an antidepressant drug takes at least 2 to 3 weeks to develop and a significant proportion of patients have no or only partial benefit regardless of the class of antidepressant used. Research into the neurobiological basis of antidepressant action has suggested new strategies to improve the antidepressant effect. Recent microdialysis studies show that hypofunction of the presynaptic autoreceptors enhances the increase of extracellular serotonin (5-HT) induced by selective serotonin reuptake inhibitors (SSRIs) so it has been suggested that the antidepressant effect may be speeded up by blockade of the autoreceptors. The similarity between the synaptic mechanisms controlling serotonergic and noradrenergic transmission has stimulated preclinical research into the role of presynaptic alpha(2)-adrenoceptors in the effect of noradrenaline (NA) reuptake inhibitors (NRIs) on NA availability at central synapses. The microdialysis studies reviewed here indicate that NRIs including desipramine, reboxetine and atomoxetine, the mixed 5-HT/NA reuptake inhibitors sibutramine, duloxetine, venlafaxine or the NA/DA reuptake inhibitor amineptine, increased extracellular NA in various regions of the rat brain. The effect was enhanced by chronic treatment and even more by the co-administration of alpha(2)-adrenoceptor antagonists. The results support the theory that desensitization of the alpha(2)-adrenoceptor contributes to enhancing the effect of NRIs seen after chronic administration and may account for the slow onset of the antidepressant effect. Finally, they suggest that co-administration of an alpha(2)-adrenoceptor antagonist may improve the therapeutic effect of NRI.


I knowm this idea has been kicked around for a long time, and that alpha-2 antagonism had an adverse effect on you, but that might have been idiosyncratic to the drug you were on (e.g. atomoxetine induces depression in me invariably now, although it didn't at first, while nortriptyline continues to be well-tolerated).

I also notice that Abilify has a long half-life, while buspirone is metabolized rapidly and thus might be conjectured to produce a more fleeting effect on 5-HT 1A receptors. Nonetheless I remember reading in a book that I consider highly ("The Antidepressant Era" by David Healy) that 5-HT 1A agonists are pro-sexual and promote orgasm. Of course the only 5-HT 1A agonist in wide use at time of writing was buspirone itself, and buspirone is the most erratic of psychotropics. So who knows... anyway, please report on your experiment.

-z


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