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Dr. Bob is Robert Hsiung, MD,
bob@dr-bob.orgShown: posts 1 to 5 of 5. This is the beginning of the thread.
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]
Posted by Bekka H. on April 27, 2002, at 1:04:33
In reply to Bekka H- Lamictal tyrosine/dopamine depletion, posted by 3 Beer Effect on April 27, 2002, at 0:37:47
Hi 3 Beers,
Thank you so much for all that information! I really appreciate it. It's good to "see" you again.
Bekka
Posted by TSA West on April 27, 2002, at 1:24:50
In reply to Bekka H- Lamictal tyrosine/dopamine depletion, posted by 3 Beer Effect on April 27, 2002, at 0:37:47
Esteemed Sir,
Thank you for that information, and dopamine depletion is a definite possibility with Lamotrigine. However, Lamotrigine's action on serotonin is overwhelmingly valuable to the bipolar and unipolar population, possibly negating any effect that Lamotrigine has on dopamine:
Southam E, Kirkby D, Higgins GA, Hagan RM. Lamotrigine inhibits monoamine uptake in vitro and modulates 5-hydroxytryptamine uptake in rats.
Eur J Pharmacol. 1998 Sep 25;358(1):19-24:
"The inhibition of the p-chloroamphetamine-induced 5-HT syndrome in rats suggests that lamotrigine also inhibits 5-HT uptake in vivo. These effects probably reflect an affinity for biogenic amine transporters..."Erfurth A, Amann B, Grunze H. Female genital disorder as adverse symptom of lamotrigine treatment. A serotoninergic effect?
Neuropsychobiology. 1998 Oct;38(3):200-1:
"The new anticonvulsant, lamotrigine, is becoming an important tool in the treatment of bipolar disorder, including bipolar depression. Its efficacy in bipolar depression might be linked to its inhibition of serotonin uptake..."Kumar TC, Khanna S.
Lamotrigine augmentation of serotonin re-uptake inhibitors in obsessive-compulsive disorder.
Aust N Z J Psychiatry. 2000 Jun;34(3):527-8.Shiah IS, Yatham LN, Lam RW, Zis AP. Effects of lamotrigine on the 5-HT1A receptor function in healthy human males.
J Affect Disord. 1998 May;49(2):157-62.--Salvation Army Adult Rehabilitation Center Command: Working through God and Al Anon to clean up your community
Posted by katekite on April 27, 2002, at 10:54:00
In reply to Bekka H- Lamictal tyrosine/dopamine depletion, posted by 3 Beer Effect on April 27, 2002, at 0:37:47
That was a great post 3beers.
I seem to have a good response to as little as 2.5 of ritalin but so far nothing to dexedrine (except decreased apetite) (although dex does stop my rebound from ritalin so it must do a little something), and am wondering how its possible. I'm trying to be cautious with the dex but so far it seems like a placebo almost.
Any thoughts? Does dex inhibit the dopamine transporter or mostly cause release? I know ritalin supposedly does not cause release but does inhibit the dopamine transporter.
This is interesting regarding dex and ritalin and serotonin, but don't have the full article so don't know what they mean by 'hi-dose':
-------
Differential effects of psychostimulants and related agents on dopaminergic and serotonergic transporter function.
Fleckenstein AE, Haughey HM, Metzger RR, Kokoshka JM, Riddle EL, Hanson JE, Gibb JW, Hanson GR.
Department of Pharmacology and Toxicology, University of Utah, 30 South 2000 East RM 201, Salt Lake City, UT, USA. fleckenstein@msscc.med.utah.edu
High-dose administrations of amphetamine, methamphetamine, cathinone, methcathinone or methylenedioxymethamphetamine rapidly decrease dopamine and serotonin transporter function in vivo, as assessed in striatal synaptosomes obtained from drug-treated rats. In contrast, high-dose injections of fenfluramine, cocaine or methylphenidate had little or no effect on the activity of these transporters. Interestingly, the capacity of these agents to directly alter dopamine and serotonin uptake, as assessed in vitro by direct application to rat striatal synaptosomes, did not predict their potential to modulate transporter activity following in vivo administration. These findings demonstrate heretofore-unreported differences in the effects of these agents on monoamine transporter function, and a distinction between drug effects after direct application in vitro vs. administration in vivo.
Posted by Dr. Bob on April 27, 2002, at 18:44:45
In reply to Re: Bekka H- Lamictal tyrosine/dopamine depletion » 3 Beer Effect, posted by TSA West on April 27, 2002, at 1:24:50
> --Salvation Army Adult Rehabilitation Center Command: Working through God and Al Anon to clean up your community
Please avoid promotional material in your tag lines:
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Thanks,
Bob
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