Posted by SLS on February 17, 2001, at 16:04:30
In reply to Re: About Mirapex, posted by AndrewB on February 17, 2001, at 13:19:14
Hi Andrew.
> Scott and I disagreed on its potential,
No.
You must surely be thinking about another Scott.
I was always well focused on the potency of Mirapex to stimulate D3 (D2 subtype) receptors in limbic structures. It more potently agonizes D3 receptors than it does D2 by a large margin. This makes this drug quite a bit different from bromocriptine in that bromocriptine is a selective D2 agonist with greater potency for that receptor than Mirapex. It seemed to me that this difference would give Mirapex greater antidepressant potential than bromocriptine. The thing that I find exciting is that you indicate that Mirapex is not as likely to poop-out. I bet the D2/D3 binding ratio is important in allowing Mirapex to provide a more persistant antidepressant response.
My thoughts regarding bromocriptine is that it is probably more effective to treat hyperprolactinemia due to its more potent D2 stimulatory effects in the pituitary gland. I have not seen Mirapex used this way. Perhaps Mirapex is of comparable efficacy. After all, how much is enough?
D3.
- Scott
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*** Check this out ***
Please note the timeline of the onset of effect.Pretty cool, huh?
Maybe even pertinent. :-)
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1: Mol Psychiatry 2000 Jul;5(4):378-88 Related Articles, Books, LinkOut
Selective increase of dopamine D3 receptor gene expression as a common effect of chronic antidepressant treatments.Lammers CH, Diaz J, Schwartz JC, Sokoloff P
Laboratoire de Physiologie, Universite Rene Descartes, 4 Avenue de l'Observatoire, 75006 Paris, France.
The mesolimbic dopaminergic system is a neuroanatomical key structure for reward and motivation upon which previous studies indicated that antidepressant drugs exert a stimulatory influence, via still unknown neurobiological mechanisms. Here we examined the effects of chronic administration of antidepressants of several classes (amitriptyline, desipramine, imipramine, fluoxetine and tranylcypromine) and repeated electroconvulsive shock treatments (ECT) on dopamine D3 receptor expression in the shell of the nucleus accumbens, a major projection area of the mesolimbic dopaminergic system. Short-term drug treatments had variable effects on D3 receptor mRNA expression. In contrast, treatments for 21 days (with all drugs except fluoxetine) significantly increased D3 receptor mRNA expression in the shell of nucleus accumbens; D3 receptor binding was also significantly increased by amitriptyline or fluoxetine after a 42-day treatment. ECT for 10 days increased D3 receptor mRNA and binding in the shell of nucleus accumbens. D1 receptor and D2 receptor mRNAs were increased by imipramine and amitriptyline, but not by the other treatments. The time-course of altered D3 receptor expression, in line with the delayed clinical efficiency of antidepressant treatment, and the fact that various antidepressant drugs and ECT treatments eventually produced the same effects, suggest that increased expression of the D3 receptor in the shell of nucleus accumbens is a common neurobiological mechanism of antidepressant treatments, resulting in enhanced responsiveness to the mesolimbic dopaminergic system.
PMID: 10889548
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poster:SLS
thread:53858
URL: http://www.dr-bob.org/babble/20010212/msgs/54271.html