Shameless bump
Just googled this very thing and came across this thread.
To clarify a few things, mirtazapines "knock out" effect is
not related to its 5ht2 antagonism, but its histamine type 1 receptor antagonism which it has an affinity approx 60 times stronger than 5ht2.
Just because 5ht2 is being antagonized to an extent does not mean that the whole receptor site is being blocked out. It has been showed that both agonism and antagonism at the 5ht2 receptor ligand has led to desensitization, leading to lower expression of 5ht2 receptor sites. So you would technically need a greater dose to reach the same level of tripping, not only due to mirtazapine but also due to the indirect desensitization.
The theory that mirtazapine can potentate or even cause serotonin syndrome comes from mirtazapines high affinity for the adrenergic 2 type receptor. Antagonism at this ligand has shown to increase overall neurotransmitter release(this is basically mirtazapines primary antidepressive mechanism). But if anything, this could be theoretically lethal to combine with MAO A inhibitors.
You know, the Pharmaceutical industry is really big business, and who validates drug testing anyway? Most of what we read about anti-depressants is complete bunk....
Drugs act in ways completely opposite of the way they are supposed to....drugs that antagonize ( supposedly) 5HT2 receptors....should kill a trip...or not let you trip...for me this is not true...
Clarification: You got it all wrong. In a pharmacological point of view you cannot look at a receptor individually, but instead you look at a cell containing a great exponential amount of receptors. Assuming you consume an antagonist leading to an equilibrium of about 60% receptor blockade(binding without action, i.e. antagonism), which depends completely on dosage and Ki value amongst other things, you would still have 40% of the receptors available to occupy at any time which could still successfully trigger the cellfunction. This is all assuming the antagonist and agonist both have the same kinetic affinity, which is almost never the case with 2 different compounds. But the point still stands. Now if agonist affinity is greater than antagonist which may or may not be the case with tryptamines, equilibrium will move to favor the one with greater affinity.
Bottom line is, tripping on mirta will require a dose adjustment if you wish to reach the same depth of a trip. It can also be used to kill a trip on a moderate dose(30+mg). And no there is no danger in tripping on mirta, ayahuasca excluding because i cant say for sure what effects the MAOI will have.