Posted by amigan on December 5, 2007, at 21:16:26
In reply to Re: Moclobemide Miracle » SLS, posted by Vince on August 26, 2001, at 23:30:09
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> With moclobemide, a reversible inhibitor of MAO-A (RIMA), I experienced a brief antidepressant response that was qualitatively substantially better than those I had experienced with Parnate and Nardil and more similar to that of clorgyline. Unfortunately, within a week, it exacerbated my depression to a degree so horrendous that I remained motionless and curled up into a fetal position, moaning and wimpering for days. It was easily the worst I had ever felt. I have some thoughts as to why this occured, and perhaps why moclobemide rarely seems to "stick". It has been my belief over the last 18 years that alterations in dopaminergic neurotransmission are critically involved in the etiology of my illness (unremitting bipolar II type depression with mania occuring only in association with drug exposure). I found an abstract on Medline that suggests that moclobemide promotes a passive release of dopamine from neuron terminals. This might be the mechanism by which it allows for relapse and exacerbation of depression. I imagine that such a continuous "leakage" of dopamine from the neuron eventually leads to neurotransmitter depletion, especially when such an increase in synaptic dopamine "noise" could further reduce presynaptic vesicular output via negative feed-back inhibition of DA synthesis directed by autoreceptor stimulation.
Hello.
I have searched the net to find information about this subject. but couldn't find anything. On the contrary, i have found that Moclobemide can be safely administrated to depressed parkinson patients.
Could anyone provide me a link about Moc and DA depletion?
poster:amigan
thread:75749
URL: http://www.dr-bob.org/babble/20071204/msgs/799006.html