So who here has is on an irreversible MAOI?
I'm a few days into 40MG Parnate with 75mg Nortiprtyline.
For those of us with Anhedonia this is promising as it increases dopamine in areas linked to Anhedonia, the limbic, nucleus accumbens, and the augmentation of Nortriptyline increases dopamine in the PFC, as well as potent NRI action
which blocks the tyramine diet requirement.
Source:
http://www.ncbi.nlm..../pubmed/7931221
Reboxetine prevents the tranylcypromine-induced increase in tyramine levels in rat heart.
This study aimed to examine whether the increase in heart radioactivity levels after intravenous injection of 14C-tyramine to rats pretreated with the irreversible MAO inhibitor tranylcypromine could be antagonized by reboxetine, a potent and selective noradrenaline uptake blocker. Reboxetine was found totally to abolish the effect of tranylcypromine. Heart radioactivity levels after reboxetine and tranylcypromine were very similar to those found when tyramine was injected after reboxetine only. These results suggest that reboxetine might be advantageously combined with tranylcypromine, or any MAO inhibitor, in depressed patients unresponsive of either treatment given alone.
http://www.ncbi.nlm....pubmed/10881043
Tranylcypromine, but not moclobemide, prolongs the inhibitory action of dopamine on midbrain dopaminergic neurons: an in vitro electrophysiological study.
The degradation of dopamine by monoamine oxidase (MAO) enzymes plays an important role in the function of dopamine receptors in the central nervous system. Accordingly, it has already been reported that the blockade of MAO by specific inhibitors prolongs the effects of dopamine on its receptors. By using intracellular electrophysiological recordings, here we report that the irreversible MAO A and B inhibitor tranylcypromine, but not the reversible MAO A inhibitor moclobemide, potentiates DA responses in rat midbrain dopaminergic neurones maintained in vitro. Moclobemide was not effective even when the MAO B enzymes were additionally blocked by the MAOI deprenyl. Thus, our electrophysiological findings confirm that the degradation DA is very important to control the effects of this catecholamine at a cellular level. Furthermore, they demonstrate that tranylcypromine potentiates DA neurotransmission while moclobemide is devoid of dopaminergic action in an in vitro condition. The phenomena reported above support the hypothesis that part of the antidepressant and antiparkinsonian effects of tranylcypromine depend on an action on DA transmission.
Interestingly, Tranylcypromine (Parnate) increases DA transmission more than even Selegiline, which i found unpleasant when i tried it.
I'm quite surprised to have minimal side effects with this combo. It feels clean and not druggy. Less so than SSRIs, and these are old drugs.
The initial effect which im told will go away, is the afternoon fatigue, and sexual side effects.
Any other experiences?
Edited by jaiho, 03 November 2015 - 10:58 PM.