Posted by zeugma on October 30, 2006, at 16:06:38
In reply to Re: Trying Emsam., posted by linkadge on October 30, 2006, at 8:35:47
> Supposedly some of the TCA's have affinity for MAO-b. I remember reading that amitryptaline either directly inhibits MAO-B, or leads to a functional inhibition of MAO-B.>>
And nortriptyline has identical MAO-B inhibiting (it is small, but direct) potential as amitriptyline.
I would guess that there is a functional inhibition as well, in that dopamine and probably PEA have an affinity for the norepinephrine transporter, and the MAO enzyme degrades the transmitter after it enters the cell. So blocking the transporting step leaves MAO with less substrate to degrade (I hope I'm getting this right).
It is conjectured that TCA's, and possibly AD's in general, are functional inhibitors (meaning the effect is downstream, as opposed to actually blocking a receptor or enzyme) of the NMDA receptor. That is why zinc is conjectured to be a good augmentor of AD's.
Passing on to Emsam,
I would think transdermal selegiline, compared to the oral route, would have a much more delayed effect, because most of selegiline's immediate effect is mediated through its amphetamine metabolites and the patch increases the parent-to-metabolite ratio.That is why 6mg/day Emsam apparently inhibits enough MAO-A to have an AD effect, while orally afministered selegiline requires over 10 mg/day to lose selectivity for MAO-B.
I am curious to know if Emsam has any subjectively similar effects to clorgyline (a structurally related MAO-A inhibitor).
-z
>
> Linkadge
poster:zeugma
thread:698340
URL: http://www.dr-bob.org/babble/20061028/msgs/699093.html