Posted by Larry Hoover on January 13, 2005, at 10:29:09
In reply to Re: Methamphetamine vs N-acetyl-l-cysteine, posted by chemist on January 13, 2005, at 0:21:49
Thanks for stepping up.
> ...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?
> 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.
Do you have a link?
> 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
>Only one thing left out. How does NAC/glutathione fit into this all?
Lar
poster:Larry Hoover
thread:439943
URL: http://www.dr-bob.org/babble/20050113/msgs/441564.html