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Re: SSRI Induced HPTA Disruption

Posted by SLS on February 8, 2009, at 8:56:19

In reply to Re: SSRI Induced HPTA Disruption, posted by linkadge on February 7, 2009, at 17:43:27

> SSRI's tend to increase the respsivness of dopamine d3 receptors. 3 week treatemtns with SSRI's, TCA's and ECT increase d3 receptor mRNA in certain limbic brain regions. Whether this is (as some suggest) a common target of antidepressive agents or simply an upregulation in responce to decrease dopaminergic function is unknown.

If desipramine, which is practically specific for NET, were to produce the same upregulation of D3 receptors, then I would say that there is something going on there other than compensations for changes in synaptic concentrations of ligand. Apparantly, it does. So, I think your inclinations to ascribe a persistent augmentative boost to Mirapex when combined with many different antidepressants are well supported.

This is probably an abstract that you have already come across:

- Scott


1: Mol Psychiatry. 2000 Jul;5(4):378-88.Links
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, Université René 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.




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