Posted by chemist on January 13, 2005, at 12:24:36
In reply to Re: Methamphetamine vs N-acetyl-l-cysteine » chemist, posted by Larry Hoover on January 13, 2005, at 10:29:09
hi larry et al...comments below....all the best, chemist
> Thanks for stepping up.
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> > ...also, a bit of a chicken-and-egg problem, as the oxidation of DA is likely (specifically) a result of decreased (endplate locus) expression of tyrosine hydroxylase...
>
> Another DA oxidative effect, decreased dopamine synthesis. But wouldn't that attenuate some of the other effects?*** from what i read (and surmise in general about these things) the answer is yes. the interesting ``problem'' that is lurking pertains to the anatomical as well as pharmacological specificity and effects of MA. this is a borrowed observation, by the way, and perhaps is only a ``problem'' in that i do not understand it. the studies (commencing in 1982, to the best of my knowledge) where high doses of amphetamine and derivatives were administered in rodent models (later primate) with the goal being to find out where in the brain these drug were responsible for what effect have largely nailed the areas in, well, rodent and (non-human) primate models....the subtlety in the causality remains troubling (again, to me): the dose-dependence relation with neuronal loss (temporary is the best word i can use to describe it) has been established to the point of there being little room for question, while the 5-HT end of things seems to be related to the drug(s) used.***
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> > on the radar recently (1995-current) is the role of monoamine vesicular transporter (type II), which sequesters DA from oxidative mechanisms...i have one pub (Ann. N.Y. Acad. Sci., 1025:146-150, 2004) on hand wherein this mechanism is addressed in re: MA specifically; and there is a freebie (JPET, 311:1-7, 2004) wherein microglia activation is fingered as the cause of DA receptor damage.
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> Do you have a link?**** yes, and i just checked: not a freebie (neither) unless you have a subscription (personal or institutional). i apologize for the misinformation.****
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> > i will state that mccann and ricaurte's review (Neuro. Bio. Rev., 27:821-826, 2004) is rather unbiased and the refs therein are a broad sampling from the literature. i was impressed with the MPTP challenge for rats dosed with MA, either with prior methylphenidate administration or with subsequent treatment...the methylphenidate staves off MPTP DA trouble if used prophylactically, and is somewhat of a restorative agent if used later....hope this sheds some light..all the best, chemist
> >
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> Only one thing left out. How does NAC/glutathione fit into this all?**** the involvement of NAC - good, bad, or none - is not addressed in any publications i have on hand, not even alluded to: my gut reaction is that NAC is a good thing to take for the reasons you outline - i think many of us are on the same page about antioxidants in general - yet the connection with DA is circumstantial and/or anecdotal at best. however, just because yours truly has not read an article or many does not mean the science is not being investigated. thus, off to the stacks i go....all the best, chemist ****
>
> Lar
poster:chemist
thread:439943
URL: http://www.dr-bob.org/babble/20050113/msgs/441625.html