Posted by pat c. on November 4, 2001, at 8:33:04
In reply to Re: Inhibition of MAO-B Increases GABA, posted by JGalt on November 3, 2001, at 22:33:06
Well said. Thank you for the explanation.
Is there anything we can extrapolate from this?
Is MAO-B the primary MAO to be concerned about in aypical depression, or at least the social phobia aspect of it?
Is GABA a major player in atypical depression?
Does this say anything about the effectiveness or ineffectiveness of Seligine against atypical depression?
I'm curious whether low levels of GABA can cause depression. I took Nardil, but it kept pooping out. I was on 150mg at one point, if you can believe that. I was hypomanic as hell. But the symptoms of atypical depression kept coming back. I got off Nardil, and lost 50 pounds.
I was on 3.0 mg of Klonopin (a GABA agent), and I've gotten off most of that. I could really use the 3mg back. I wonder why Klonopin is so effective against atypical depression. It obviously solves the GAD, panic, and social phobia aspects of the disease. I'm also beginning to think Klonopin might have antidepressant action.
Currently, I'm on 0.25 of Klonopin (down from 0.5 mg last week) and 1600 of Neurontin (down from 4800 two months ago). I'm having a rough time getting off these two drugs. This week's 0.25 cut in Klonopin is hell. I'm ramping back up the Neurontin to counteract the Klonopin cut.
Lowering the levels of Neurontin (another GABA agent) has been quite difficult. I'm not sure whether Neurontin is just an augmenting agent, or whether it can be used by itself. I'll find out.
Meanwhile, the depression aspect on my atypical depression is getting worse.
Obviously, I'm looking for answers, so I'm persuing this GABA angle. It seems to be the common denominator between Nardil, Klonopin and Neurontin. I need a drug for atypical depression other than Nardil (made me too fat) and Klonopin (history of addiction).
I believe there are five possible reasons for my atypical depression (social phobia, anxiety attacks, and depression):
1) GABA (inhibiting neurotransmitter) level too low
2) Glutamate (excitatory neurotransmitter) level too high
3) Serotonin (inhibitor) level too low
4) Dopamine (excitatory) level too high
5) Norepinephrine (excitatory) level too highSerotonin reuptake inhibitors didn't help, so I'm writing off the Serotonin angle, although I'm curious about FDA testing of Gepirone, which is getting good reviews.
Lowering Glutamate with Lamactil caused major memory problems.
I've has some success in increasing GABA.
I get anxiety attacks from dopamine agents like Wellbutrin and Ritalin, which makes me think that I have too much Dopamine, and since norepinephrine is formed from Dopamine, perhaps I have too much norepinephrine.Any thoughts would be helpful.
Thank you for your time.
Pat
poster:pat c.
thread:83124
URL: http://www.dr-bob.org/babble/20011104/msgs/83158.html