Dextromethorphan is a dopamine reuptake inhibitor..this is a bit of the limited research Ive done

http://en.wikipedia.org/wiki/Dextromethorphan

http://en.wikipedia.org/wiki/Dopamin...take_inhibitor

http://www.nlm.nih.gov/medlineplus/d...di/202187.html

I read about dextromethorphan with a lot of interest as, like Steve, my symptoms are progressing a bit too rapidly for my liking! But from the Wikipedia description of how it works, it looks like it's just increasing the amount of dopamine in the brain. Wouldn't that be just like taking a bit more Sinemet?

I put your review onto a word document, spell checked it [ignored names - had no idea], and emailed it to Dr. Todd Sherer at Fox Foundation, reminded him that I had asked about it at PAN, and asked for an opinion; also mentioned for him to feel free to share with any colleagues.

We'll see what type of response it draws. None wouldn't be good.

thanks!

Paula

I dont really understand all that takes place, but it was explained to me that normally for the dopamine signal to respond for movement is like switching the lights on..and when you have a dopamine reuptake inhibitor working its like the lights are always on, and that is the force behind what I think seems to be working for me

Paula,
Thanks for your consistent support, I look forward to hearing n his reaction.

Has anyone done a search on dextromethorphan, as to its effect on the BBB??
Ron

When I first heard about this cough syrup I went out to buy some but U.K cough medication does not seem to contain Dextromethorphan unless it has another name.

thanks for the infor about MAOB inhibitors and dextromethorphan--is that not the ingredient some youth use to get high? seems I read that recently. also, the following is from another post that also belongs here:
BBB and glutathione peroxidase + glial cells

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Perhaps with disruption of the BBB, the area of the substantia nigra is most susceptible to damage from toxins, infectious agents etc, partially owing to the fact that the lowest density of glutathione peroxidase postitive glial cells is found in the substantia nigra, rendering this dopaminergic cell group less protected and more susceptible to oxidative stress and thus vulnerable to Parkinson’s disease.

Dextromethorphan is an ingredient in the home brew of methamphetamine which is the reason it can be hard to find. The report below shows its promise. However, I have not been able to find that it gets past the BBB nor that it affects the BBB itself. Doesn't mean it doesn't, just that no clear study popped up.


1: J Pharmacol Exp Ther. 2003 Apr;305(1):212-8.

Dextromethorphan protects dopaminergic neurons against inflammation-mediated
degeneration through inhibition of microglial activation.

Liu Y, Qin L, Li G, Zhang W, An L, Liu B, Hong JS.

Laboratory of Pharmacology and Chemistry, National Institute of Environmental
Health Sciences, Research Triangle Park, North Carolina 27709, USA.

Inflammation in the brain has increasingly been recognized to play an important
role in the pathogenesis of several neurodegenerative disorders, including
Parkinson's disease and Alzheimer's disease. Inflammation-mediated
neurodegeneration involves activation of the brain's resident immune cells, the
microglia, which produce proinflammatory and neurotoxic factors, including
cytokines, reactive oxygen intermediates, nitric oxide, and eicosanoids that
impact on neurons to induce neurodegeneration. Hence, identification of
compounds that prevent microglial activation may be highly desirable in the
search for therapeutic agents for inflammation-mediated neurodegenerative
diseases. In this study, we report that dextromethorphan (DM), an ingredient
widely used in antitussive remedies, reduced the inflammation-mediated
degeneration of dopaminergic neurons through inhibition of microglial
activation. Pretreatment (30 min) of rat mesencephalic neuron-glia cultures with
DM (1-10 micro M) reduced, in a dose-dependent manner, the microglia-mediated
degeneration of dopaminergic neurons induced by lipopolysaccharide (LPS, 10
ng/ml). Significant neuroprotection by DM was also evident when DM was applied
to cultures up to 60 min after the addition of LPS. The neuroprotective effect
of DM was attributed to inhibition of LPS-stimulated microglial activation
because DM significantly inhibited the LPS-induced production of tumor necrosis
factor-alpha, nitric oxide, and superoxide free radicals. This conclusion was
further supported by the finding that DM failed to prevent
1-methyl-4-phenylpyridinium- or beta-amyloid peptide (1-42)-induced dopaminergic
neurotoxicity in neuron-enriched cultures. In addition, because LPS did not
produce any significant increase in the release of excitatory amino acids from
neuron-glia cultures and N-methyl-D-aspartate antagonist dizocilpine maleate
failed to afford significant neuroprotection, it is unlikely that the
neuroprotective effect of DM is mediated through N-methyl-D-aspartate receptors.
These results suggest that DM may be a promising therapeutic agent for the
treatment of Parkinson's disease.

PMID: 12649371 [PubMed - indexed for MEDLINE]

from wikipedia:

Clinical pharmacology
Following oral administration, dextromethorphan is rapidly absorbed from the gastrointestinal tract, where it enters the bloodstream and crosses the blood-brain barrier. The first-pass through the hepatic portal vein results in some of the drug being metabolized into an active metabolite of dextromethorphan, dextrorphan, the 3-hydroxy derivative of dextromethorphan. The therapeutic activity of dextromethorphan is believed to be caused by both the drug and this metabolite. Dextromethorphan is metabolized by various liver enzymes and subsequently undergoes O-demethylation (producing dextrorphan), N-demethylation, and partial conjugation with glucuronic acid and sulfate ions. Hours after dextromethorphan therapy, (in humans) the metabolites (+)-3-hydroxy-N-methylmorphinan, (+)-3-morphinan, and traces of the unchanged drug are detectable in the urine.[5]
A major metabolic catalyst involved is the cytochrome P450 enzyme known as 2D6, or CYP2D6. A significant portion of the population has a functional deficiency in this enzyme and are known as poor CYP2D6 metabolizers. As CYP2D6 is a major metabolic pathway in the inactivation of dextromethorphan, the duration of action and effects of dextromethorphan can be increased by as much as three times in such poor metabolizers.[6]
A large number of medications (including antidepressants) are potent inhibitors of CYP2D6 (see CYP2D6 article). There exists, therefore, the potential of interactions between dextromethorphan and concomitant medications. There have been reports of fatal consequences arising from such interactions.[7]
Dextromethorphan crosses the blood-brain barrier, and the following pharmacological actions have been reported:

• NMDA glutamatergic receptor antagonist
• Dopamine reuptake inhibitor[5]
• σ1 and σ2 receptor agonist.[8]
• α3β4 nicotinic receptor antagonist[9]
• Serotonin reuptake inhibitor[10]

Dextromethorphan is used as a cough suppesant and is found in Robitussin and other cough medicines