Posted by 3 Beer Effect on April 27, 2002, at 0:37:47
No one really knows how Lamictal works but I think it may lower dopamine levels, although medical studies often contradict each others findings.
I found one study that I printed below that says Lamictal may inhibit tyrosine hydroxylase. Tyrosine hydroxylase is what transforms L-tyrosine to L-Dopa & then other steps occur eventually creating Dopamine then Norepinephrine, then epinephrine. So it is possible that Lamictal may lower your body's potential to create dopamine.
I have a hunch that Lamictal is interfering with the stimulant activity of the Dexedrine (Dextrostat) I am taking. I am now taking 20 mg twice per day but am hardly even feeling it. I used to take Klonopin but stopped to see if it was the Klonopin that was blunting the Dexedrine but it wasn't. This week I am titrating the Lamictal to 175 mg, and will go to 200 mg the week after that because it hasn't had any effect on my depression yet at 150 mg even though i've been on it for about 3 months.
From other things I have read, serotonin & dopamine are kind of like a see-saw and keep each other in balance. So most medications that raise serotonin will decrease dopamine & vice versa (with the possible exception of Zoloft which has slight dopamine reuputake inhibition properties).
I noticed with mood-stablizers, they often inhibit the action of amphetamines but do not inhibit the action of Ritalin or Cocaine. I think this is because amphetamines are more dependent on synthesis, storage and release of dopamine while Ritalin & Cocaine simply block the reuputake of Dopamine. One study I read said that Lamictal blunted the excitatory effects of methamphetamine while in another study Lamictal did not have any effect on the subjective effects of Cocaine. Ritalin acts in a remarkably similar way to Cocaine, it is often called "kiddie Cocaine" on the street, but since Ritalin clears from the brain at a much slower rate it is not as reinforcing & doesn't lead to constant readministration & addiction as often as Cocaine does.
I am giving the 20 mg 2x per day Dextrostat a one month trial but I remember I could concentrate much better 18 months ago when I took 20 mg of Ritalin 2x per day. The Ritalin seemed much more powerful than the Dextrostat does now which does not make any sense since 10 mg of Dextrostat/Dexedrine is supposed to equal 20 mg of Ritalin since Dextroamphetamine is twice as potent. It has dawned on me that when I was taking Ritalin I wasn't taking an anti-depressant or any other medication. So now I am taking 20 mg per dose of Dextrostat which according to any psychiatry textbook equals a 40 mg dose of Ritalin, but still seems weaker than 20 mg of Ritalin! So then Lamictal (150 mg) is probably the culprit & is blunting the Dextrostat.
Since Lamictal does not change the effects of Cocaine, I bet that it would not effect Ritalin either, so I will probably switch back to Ritalin, try Concerta, or better yet try the new & improved Ritalin called Focalin which contains only the active d-isomer (Ritalin is racemic, with an active d isomer and a totally inactive/worthless l-somer). 10 mg of Focalin= 20 mg of Ritalin & so your liver & kidneys don't have to process that 10 mg of worthless filler.
Here is the study you were looking for:"Lamotrigine inhibits the in situ activity of tyrosine hydroxylase in striatum of audiogenic seizure-prone and audiogenic seizure-resistant Balb/c mice".
Vriend J, Alexiuk NA.
Department of Anatomy, University of Manitoba, Winnipeg, Canada.
Lamotrigine (LTG), an anticonvulsive drug, was tested for its effects on striatal content of DA and its metabolites, DOPAC and HVA, in audiogenic seizure-resistant (ER) and audiogenic seizure-prone (EP) lines of Balb/c mice. A single dose of LTG (20 mg/kg) prevented audiogenic seizures in seizure-prone mice, while reducing substantially the striatal content of the DA metabolite, DOPAC (to less than 50% of saline-injected controls) in both seizure-resistant and seizure-prone mice. LTG administration also resulted in significant reduction of striatal content of HVA. The in situ activity of tyrosine hydroxylase (TH) in extracts of striatum was significantly reduced by LTG administration in both ER and EP mice. These data show that DA synthesis in the striatum of mice is substantially reduced by LTG administration.
PMID: 9416765 [PubMed - indexed for MEDLINE]
poster:3 Beer Effect
thread:104261
URL: http://www.dr-bob.org/babble/20020425/msgs/104261.html