Posted by undopaminergic on September 17, 2021, at 12:10:28
In reply to Re: Help..severe anger.... » SLS, posted by undopaminergic on September 17, 2021, at 8:22:53
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> > > Just to clarify, I'm wondering why specific MAO-A inhibition with clorgyline would be better than dual MAO-A and MAO-B inhibition with classic MAOIs. MAO-B contributes to dopamine breakdown, so one would think that inhibiting it in addition to MAO-A would be beneficial, rather than the opposite, that is MAO-B inhibition being detrimental.
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> > I'm sure there is a biological reason for why we see this.
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> My best theory is as follows: MAO-B has been called phenylethylaminase, because its primary substrate is phenylethylamine (PEA), which at higher concentrations works like amphetamine. Thus PEA releases dopamine (and noradrenaline and maybe serotonin) from dopaminergic nerve terminals. This may result in a sensitation of dopamine autoreceptors, reducing dopamine synthesis and release. This may result in a functional depressive (apathetic, etc.) effect. So I wonder whether adding sulpiride or amisulpride would help.
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> But: PEA administered during MAO-B inhibition in sufficient quantities yields a powerful antidepressant (or stimulant) effect.
>Alternative theory: there could be a MAO-B substrate that is depressogenic. It may be hitherto unidentified as a MAO-B target.
MPTP is a neurotoxin that produces Parkinson's disease. It is actually a precursor to the actual toxin; MAO-B converts MPTP to the MPP+ ion. There could be some other toxin that produces depression rather than Parkinson's, and which is *inactivated* by MAO-B, so that if you inhibit MAO-B, this substance is let loose on the CNS.
-undopaminergic
poster:undopaminergic
thread:1116908
URL: http://www.dr-bob.org/babble/20210723/msgs/1116981.html