Posted by AndrewB on August 7, 2000, at 11:39:47
In reply to Re: Adrafinil, anyone experience this?, posted by JohnL on August 7, 2000, at 3:59:26
John,
Thanks for all the great advice. I will try to give adrafinil a fair trial.
I am going to halt the adrafinil trial until I receive some propranolol for the headcahes. Then I will go with 150mgs/day to start.
How long does it take for the adrafinil to leave your system? Can you believe it, I felt an arousal effect from adrafinil in a few hours!
Make note that Michael is using bromocriptine successfully to combat adrafinil induced sexual dysfunction. I have also read that bromocriptine is effective for amisulpride sexual dysfunction. Seems to me that if you took bromcriptine you may be able to take both amisulpride and adrafinil together again.
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Scott,I don't know if Naphazoline crosses the blood brain barrier. On a related note, I am very interested in the idea of an alphal1 andrenergic agonist being able to be centrally selective in its actions (vs. having both central and periphereal action) as is claimed (hah, hah!) for adrafinil. Reboxetine's effect of severely limiting my athletic stamina and the sexual side effects, I believe are due to periphereal alpha1 agonism. So I would think a centrally acting alpha1 agonist would be great for a lot of people, myself included.
Glutamate opens the calcium channels. Compare this to the calcium channel blocking action of nimodipine. Too much calcium within the cell somehow leads to neuron death. I forgot the speicifics. Anyway, such glutamate induced neuron death is being recognized as a leading factor in a lot mental maladies and other conditions. For example, the greater part of the brain damage caused by a stroke is not due to hypoxia, rather glutamate toxicity. By applying a drug that blocks glutamate's action soon after a stroke, such as a calcium channel blocker, people have been able to recover much better from strokes. It is Memantine's glutamate limiting actions, as an NMDA receptor antagonist, that enables it to be effective in the treatment of dementia, neuropathic pain, Alzheimers, Huntington's disease, Amyotrophic Lateral Sclerosis and glaucoma. The miracles of modern medicine!
Now Scott, let me ask you, how do you think lamotrigine's glutamate lowering action translates into its effectiveness as a mood stabilizer. And is there a relationship between the glutamate effect limiting action of a calcium channel blocker like nimodipine and the calcium channel blocker's effectiveness as an augmenting agent to mood stabilizers. Have you ever considered taking a mood stabilizer?
As far as Provigil and glutamate toxicity, that is just a loose thought of mine. I would be more comfortable with adrafinil and Provigil if their mechanisms of action were better understood.
I'm not sure why reboxetine pooped out. The timing of it though clears selegiline of any association with it. Actually, I quickly built up a tolerance to Naphazoline (the alpha1 agonist) and this tolerance seems also to have crossed over and effected reboxetine's ability to act on these receptors. But, hey, I wouldn't lay money down on that being what really happened.
One final note, Dr. Goldstein lists neurontin as an (indirect) NMDA antagonist.
Best wishes to the both of you,
AndrewB
poster:AndrewB
thread:42223
URL: http://www.dr-bob.org/babble/20000729/msgs/42335.html